Researcher Profile - Yoshihiro Ishikawa

写真a

Yoshihiro Ishikawa

Organization

President,etc. President

Homepage

https://www.yokohama-cu.ac.jp/univ/outline/message/index.html

Profile

専門は循環制御医学。米国大学(複数）において、医学生、教員および医師、日米欧において科研費審査委員、学術雑誌の編集委員を務める。横浜市立大学大学院医学研究科長、医学群長、副学長等を経て２０２４年より横浜市立大学学長（現職）。

External link

Degree

博士（医学） ( 横浜市立大学 )

Research Interests

アデニル酸シクラーゼ
循環制御
cAMP
カベオリン
カテコラミン
自律神経
心不全
遺伝子操作
インシュリン
医療安全管理
米国医療制度
遺伝子治療
アデノウイルス
心臓
カルシウム
ノックアウト
交感神経
心臓型
フォルスコリン
ファルマコ分析
ニコチン受容体
糖尿病
PKA
magnetic drug
anti-cancer drug
ドーパミン
アポプトーシス
G蛋白質
統合脳・病態脳

Research Areas

Life Science / Physiology
Life Science / Tumor diagnostics and therapeutics
Life Science / Pharmacology
Life Science / Clinical pharmacy
Life Science / Cardiology

Research History

Yokohama City University Office of the President President

2024.4

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横浜市立大学医学研究科教授

1998 - 2024

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Drexel University Medical School Associate Professor

1997

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Harvard University

1995 - 1997

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Columbia University

1991 - 1995

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Massachusetts General Hospital Cardiac Unit Research Fellow

1988 - 1990

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Professional Memberships

日本循環制御医学会

2005

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日本心臓病学会

2004

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日本心血管内分泌代謝学会

1999

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European Society of Cardiology

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American Physiological Society

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American College of Cardiology

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American College of Physicians

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American Heart Association

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Committee Memberships

横浜市環境影響評価審査会委員

2023 - 2024.3

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Committee type：Municipal

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日本生理学会理事長

2020 - 2024.3

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Committee type：Academic society

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日本学術振興会基盤研究S 評価協力者

2020 - 2021

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ツールーズ大学（フランス）研究評価者 Initiative of Excellence Program

2015

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Committee type：Other

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東京医科歯科大学難治疾患研究所教員活動評価委員会外部委員

2014

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Committee type：Other

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アメリカ生理学会国際生理学委員会

2013 - 2015

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Committee type：Academic society

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日本学術センター医歯薬専門調査班・専門調査委員

2012 - 2015

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Committee type：Government

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自然科学研究機構生理学研究所運営会議委員

2012 - 2014

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Committee type：Government

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日本病態代謝学会理事

2010

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Committee type：Academic society

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日本生理学会常任幹事・理事・副理事長

2008 - 2020

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Committee type：Academic society

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日本循環制御医学会理事

2005

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Committee type：Academic society

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日本学術振興会科学研究費委員会専門委員基盤研究S

2022 - 2024

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国公私立大学図書館協力委員会委員長

2022 - 2023

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公益財団法人佐藤陽国際奨学財団選考委員

2021

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横浜市横浜サイエンスフロンティア高等学校科学技術顧問

2020

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名古屋市立大学特別研究奨励賞課題評価委員

2020 - 2024

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Committee type：Municipal

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日本心臓病学会代議員

2020 - 2022

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日本学術振興会科学研究費委員会専門委員基盤研究A

2019 - 2022

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日本宇宙航空環境医学会評議員

2018 - 2024

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自然科学研究j機構生理学研究所外部評価委員

2017

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Committee type：Academic society

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日本内分泌学会代議員

2013

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Committee type：Academic society

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日本薬理学会評議員

2012

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Committee type：Academic society

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国際心臓研究学会評議員

2012 - 2024

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Committee type：Academic society

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文部科学省科学研究費委員会専門委員・生理学一般

2011 - 2012

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Committee type：Government

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日本臨床生理学会評議員

2007

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Committee type：Academic society

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文部科学省研究費委員会専門委員・循環器内科

2006 - 2008

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Committee type：Government

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日本心不全学会評議員

2004 - 2010

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Committee type：Academic society

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日本心血管内分泌代謝学会評議員

2000

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Committee type：Academic society

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日本循環器学会評議員

2000 - 2019

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Committee type：Academic society

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日本心電学会評議員

2000 - 2006

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Papers

Fibulin-1 Integrates Subendothelial Extracellular Matrices and Contributes to Anatomical Closure of the Ductus Arteriosus. International journal

Satoko Ito, Utako Yokoyama, Taichi Nakakoji, Marion A Cooley, Takako Sasaki, Sonoko Hatano, Yuko Kato, Junichi Saito, Naoki Nicho, Shiho Iwasaki, Masanari Umemura, Takayuki Fujita, Munetaka Masuda, Toshihide Asou, Yoshihiro Ishikawa

Arteriosclerosis, thrombosis, and vascular biology 40 ( 9 ) 2212 - 2226 2020.9

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Language：English Publishing type：Research paper (scientific journal)

OBJECTIVE: The ductus arteriosus (DA) is a fetal artery connecting the aorta and pulmonary arteries. Progressive matrix remodeling, that is, intimal thickening (IT), occurs in the subendothelial region of DA to bring anatomic DA closure. IT is comprised of multiple ECMs (extracellular matrices) and migrated smooth muscle cells (SMCs). Because glycoprotein fibulin-1 binds to multiple ECMs and regulates morphogenesis during development, we investigated the role of fibulin-1 in DA closure. Approach and Results: Fibulin-1-deficient (Fbln1-/-) mice exhibited patent DA with hypoplastic IT. An unbiased transcriptome analysis revealed that EP4 (prostaglandin E receptor 4) stimulation markedly increased fibulin-1 in DA-SMCs via phospholipase C-NFκB (nuclear factor κB) signaling pathways. Fluorescence-activated cell sorting (FACS) analysis demonstrated that fibulin-1 binding protein versican was derived from DA-endothelial cells (ECs). We examined the effect of fibulin-1 on directional migration toward ECs in association with versican by using cocultured DA-SMCs and ECs. EP4 stimulation promoted directional DA-SMC migration toward ECs, which was attenuated by either silencing fibulin-1 or versican. Immunofluorescence demonstrated that fibulin-1 and versican V0/V1 were coexpressed at the IT of wild-type DA, whereas 30% of versican-deleted mice lacking a hyaluronan binding site displayed patent DA. Fibulin-1 expression was attenuated in the EP4-deficient mouse (Ptger4-/-) DA, which exhibits patent DA with hypoplastic IT, and fibulin-1 protein administration restored IT formation. In human DA, fibulin-1 and versican were abundantly expressed in SMCs and ECs, respectively. CONCLUSIONS: Fibulin-1 contributes to DA closure by forming an environment favoring directional SMC migration toward the subendothelial region, at least, in part, in combination with EC-derived versican and its binding partner hyaluronan.

DOI： 10.1161/ATVBAHA.120.314729

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Excessive EP4 Signaling in Smooth Muscle Cells Induces Abdominal Aortic Aneurysm by Amplifying Inflammation. Reviewed International journal

Taro Hiromi, Utako Yokoyama, Daisuke Kurotaki, Al Mamun, Ryo Ishiwata, Yasuhiro Ichikawa, Hiroshi Nishihara, Masanari Umemura, Takayuki Fujita, Shota Yasuda, Tomoyuki Minami, Motohiko Goda, Keiji Uchida, Shinichi Suzuki, Ichiro Takeuchi, Munetaka Masuda, Richard M Breyer, Tomohiko Tamura, Yoshihiro Ishikawa

Arteriosclerosis, thrombosis, and vascular biology 40 ( 6 ) ATVBAHA120314297 - 1573 2020.4

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OBJECTIVE: Excessive prostaglandin E2 production is a hallmark of abdominal aortic aneurysm (AAA). Enhanced expression of prostaglandin E2 receptor EP4 in vascular smooth muscle cells (VSMCs) has been demonstrated in human AAAs. Although moderate expression of EP4 contributes to vascular homeostasis, the roles of excessive EP4 in vascular pathology remain uncertain. We aimed to investigate whether EP4 overexpression in VSMCs exacerbates AAAs. Approach and Results: We constructed mice with EP4 overexpressed selectively in VSMCs under an SM22α promoter (EP4-Tg). Most EP4-Tg mice died within 2 weeks of Ang II (angiotensin II) infusion due to AAA, while nontransgenic mice given Ang II displayed no overt phenotype. EP4-Tg developed much larger AAAs than nontransgenic mice after periaortic CaCl2 application. In contrast, EP4fl/+;SM22-Cre;ApoE-/- and EP4fl/+;SM22-Cre mice, which are EP4 heterozygous knockout in VSMCs, rarely exhibited AAA after Ang II or CaCl2 treatment, respectively. In Ang II-infused EP4-Tg aorta, Ly6Chi inflammatory monocyte/macrophage infiltration and MMP-9 (matrix metalloprotease-9) activation were enhanced. An unbiased analysis revealed that EP4 stimulation positively regulated the genes binding cytokine receptors in VSMCs, in which IL (interleukin)-6 was the most strongly upregulated. In VSMCs of EP4-Tg and human AAAs, EP4 stimulation caused marked IL-6 production via TAK1 (transforming growth factor-β-activated kinase 1), NF-κB (nuclear factor-kappa B), JNK (c-Jun N-terminal kinase), and p38. Inhibition of IL-6 prevented Ang II-induced AAA formation in EP4-Tg. In addition, EP4 stimulation decreased elastin/collagen cross-linking protein LOX (lysyl oxidase) in both human and mouse VSMCs. CONCLUSIONS: Dysregulated EP4 overexpression in VSMCs promotes inflammatory monocyte/macrophage infiltration and attenuates elastin/collagen fiber formation, leading to AAA exacerbation.

DOI： 10.1161/ATVBAHA.120.314297

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Prostaglandin E2 receptor EP4 regulates cell migration via Orai1. Reviewed International journal

Osawa K, Umemura M, Nakakaji R, Tanaka R, Islam RM, Nagasako A, Fujita T, Yokoyama U, Koizumi T, Mitsudo K, Ishikawa Y

Cancer science 111 ( 1 ) 160 - 174 2019.11

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The EP4 prostanoid receptors are one of four receptor subtypes for prostaglandin E2 (PGE2 ). Therefore, EP4 may play an important role in cancer progression. However, little information is available regarding their function per se, including migration and the cellular signaling pathway of EP4 in oral cancer. First, we found that mRNA and protein expression of EP4 was abundantly expressed in human-derived tongue squamous cell carcinoma cell lines HSC-3 and OSC-19. The EP4 agonist (ONO-AE1-437) significantly promoted cell migration in HSC-3 cells. In contrast, knockdown of EP4 reduced cell migration. Furthermore, we confirmed that knockdown of EP4 suppressed metastasis of oral cancer cells in the lungs of mice in vivo. Therefore, we focused on the mechanism of migration/metastasis in EP4 signaling. Interestingly, EP4 agonist significantly induced intracellular Ca2+ elevation not in only oral cancer cells but also in other cells, including normal cells. Furthermore, we found that EP4 activated PI3K and induced Ca2+ influx through Orai1 without activation of store depletion and stromal interaction molecule 1 (STIM1). Immunoprecipitation showed that EP4 formed complexes with Orai1 and TRPC1, but not with STIM. Moreover, the EP4 agonist ONO-AE1-437 phosphorylated ERK and activated MMP-2 and MMP-9. Knockdown of Orai1 negated EP4 agonist-induced ERK phosphorylation. Taken together, our data suggested that EP4 activated PI3K and then induced Ca2+ influx from the extracellular space through Orai1, resulting in ERK phosphorylation and promoting cell migration. Migration is regulated by EP4/PI3K/Orai1 signaling in oral cancer.

DOI： 10.1111/cas.14247

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An appropriately sized soft polyester external stent prevents enlargement and neointimal hyperplasia of a saphenous vein graft in a canine model. Reviewed International journal

Yasuda S, Goda M, Shibuya T, Uchida K, Suzuki S, Noishiki Y, Yokoyama U, Ishikawa Y, Masuda M

Artificial organs 43 ( 6 ) 577 - 583 2019.6

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Although the efficacy of external stents for vein grafts in coronary artery bypass grafting has been recognized, the ideal diameter and material of the stent remain controversial. We created a new external stent made of soft polyester mesh and performed an animal experiment using canines. Bilateral saphenous vein grafts were interposed in the bilateral common carotid artery of 10 beagles. The grafts in the left carotid artery were designated as the control group, and those in the right rolled by a soft polyester mesh external stent were designated as mesh group. Two of the 10 animals were sacrificed due to severe wound infection. The other eight were observed by echography for 6 months, and then grafts were extracted and thickness of the neointima of the grafts was measured. The control group showed 146% ± 26% postoperative enlargement of the internal diameter of the vein grafts after 6 months, whereas the mesh group showed only 115% ± 15% after the same duration (P = 0.0003). The median thickness of the neointima in the mesh group (170 µm [range: 150-190]) was significantly thinner than that in the control group (260 µm [range: 220-310], P < 0.0001). Some degree of correlation between the thickness of neointima and proportion of enlargement was noted (r = 0.518, P = 0.0024). A soft polyester mesh external stent for vein grafts successfully suppressed the enlargement of the vein grafts and thickness of the neointima after 6 months.

DOI： 10.1111/aor.13399

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Simultaneous hyperthermia-chemotherapy effect by arterial injection of Fe(Salen) for femur tumor. Reviewed International journal

Umemura M, Islam MR, Fukumura H, Sato I, Kawabata Y, Matsuo K, Nakakaji R, Nagasako A, Ohtake M, Takayuki F, Yokoyama U, Nakayama T, Eguchi H, Ishikawa Y

Cancer science 110 ( 1 ) 356 - 365 2019.1

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We previously identified a novel nanomagnetic particle, N,N'-bis(salicylidene)ethylenediamine iron [Fe(Salen)]. Fe(Salen) not only shows antitumor effects but also magnetic properties. We found that Fe(Salen) can be used for magnet-guided drug delivery and visualization of accumulated drug by magnetic resonance imaging (MRI) because of its magnetism. In addition, Fe(Salen) can generate heat by itself when exposed to an alternating current magnetic field (AMF), resulting in a hyperthermia effect. Herein, we partly elucidated the antitumor mechanism of Fe(Salen) and carried out an i.v. repeated dose toxicity study to decide the therapeutic amount. Furthermore, we evaluated the antitumor effect of selective intra-arterial injection or i.v. injection of Fe(Salen) by catheter and the hyperthermia effect of Fe(Salen) when exposed to AMF in vivo. We used a rabbit model grafted with VX2 cells (rabbit squamous cell carcinoma) on the right leg. Intra-arterial injection of Fe(Salen) showed a greater antitumor effect than did i.v. injection. The combination of Fe(Salen) intra-arterial injection and AMF exposure showed a greater antitumor effect than did either Fe(Salen) or methotrexate (MTX) without AMF exposure, suggesting that AMF exposure greatly enhanced the antitumor effect of Fe(Salen) by arterial injection by catheter. This is the first report that the effectiveness of Fe(Salen) was evaluated in the point of administration route; that is, selective intra-arterial injection by catheter. Taken together, these results indicate a new administration route; that is, selective arterial injection of Fe(Salen) by catheter, and the development of a new strategy of simultaneous hyperthermia-chemotherapy in the future.

DOI： 10.1111/cas.13851

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Acute Hyperthermia Inhibits TGF-β1-induced Cardiac Fibroblast Activation via Suppression of Akt Signaling Reviewed

Masatoshi Narikawa, Masanari Umemura, Ryo Tanaka, Takayuki Fujita, Utako Yokoyama, Tomoaki Ishigami, Kazuo Kimura, Kouichi Tamura, Yoshihiro Ishikawa

Scientific Reports 8 ( 1 ) 6277 2018.12

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DOI： 10.1038/s41598-018-24749-6

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Proteomic analysis of aortic smooth muscle cell secretions reveals an association of myosin heavy chain 11 with abdominal aortic aneurysm. Reviewed International journal

Yokoyama U, Arakawa N, Ishiwata R, Yasuda S, Minami T, Goda M, Uchida K, Suzuki S, Matsumoto M, Koizumi N, Taguri M, Hirano H, Yoshimura K, Ogino H, Masuda M, Ishikawa Y

American journal of physiology. Heart and circulatory physiology 315 ( 4 ) H1012 - H1018 2018.7

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Abdominal aortic aneurysm (AAA) is a life-threatening disease, and no disease-specific circulating biomarkers for AAA screening are currently available. We have identified a smooth muscle cell (SMC)-specific biomarker for AAA. We cultured aneurysmal tunica media that were collected from eight patients undergoing elective open-repair surgeries. Secreted proteins in culture medium were subjected to liquid chromatography/tandem mass spectrometry. Myosin heavy chain 11 (myosin-11) was identified as a SMC-specific protein in the tunica media-derived secretions of all patients. We then examined myosin-11 protein concentrations by ELISA in plasma samples from patients with AAA ( n = 35) and age-matched healthy control subjects ( n = 34). Circulating myosin-11 levels were significantly higher in patients with AAA than control subjects. The area under the receiver-operating characteristic curve (AUC) of myosin-11 was 0.77, with a specificity of 65% at a sensitivity of 91%. Multivariate logistic regression analysis showed a significant association between the myosin-11 level and presence of AAA. When the myosin-11 level was combined with hypertension, it improved the prediction of AAA (AUC 0.88) more than hypertension per se. We then investigated the correlation between aortic diameter and circulating myosin-11 levels using AAA serum samples from patients undergoing endovascular aneurysm repair ( n = 20). Circulating myosin-11 levels were significantly correlated with maximum aortic diameter. Furthermore, changes in myosin-11 concentrations from the baseline 12 mo after endovascular aneurysm repair were associated with those in aortic diameter. These data suggest that circulating levels of myosin-11, which is a SMC-specific myosin isoform, may be useful as a biomarker for AAA. NEW & NOTEWORTHY Extensive studies have revealed that inflammation- or proteolysis-related proteins are proposed as biomarkers for abdominal aortic aneurysm (AAA). Changes in these protein concentrations are not specific for smooth muscle, which is a major part of AAA pathologies. Hence, no disease-specific circulating markers for AAA are currently available. We found, using secretome-based proteomic analysis on human AAA tunica media, that myosin heavy chain 11 was associated with AAA. Circulating myosin heavy chain 11 may be a new tissue-specific AAA marker.

DOI： 10.1152/ajpheart.00329.2018

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Vidarabine, an anti-herpesvirus agent, prevents catecholamine-induced arrhythmias without adverse effect on heart function in mice Reviewed

Kenji Suita, Takayuki Fujita, Wenqian Cai, Yuko Hidaka, Huiling Jin, Rajesh Prajapati, Masanari Umemura, Utako Yokoyama, Motohiko Sato, Björn C. Knollmann, Satoshi Okumura, Yoshihiro Ishikawa

Pflugers Archiv European Journal of Physiology 470 ( 6 ) 923 - 935 2018.6

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Language：English Publishing type：Research paper (scientific journal) Publisher：Springer Verlag

DOI： 10.1007/s00424-018-2121-4

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Treatment of oral cancer using magnetized paclitaxel Reviewed

Rina Nakakaji, Masanari Umemura, Kenji Mitsudo, Jeong-Hwan Kim, Yujiro Hoshino, Itaru Sato, Takatsugu Masuda, Masahiro Yamamoto, Mitomu Kioi, Toshiyuki Koizumi, Takayuki Fujita, Utako Yokoyama, Masaki Iida, Motohiko Sato, Hiroshi Sato, Shoko Murofushi, Sayaka Shibata, Ichio Aoki, Haruki Eguchi, Iwai Tohnai, Yoshihiro Ishikawa

Oncotarget 9 ( 21 ) 15591 - 15605 2018

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Language：English Publishing type：Research paper (scientific journal) Publisher：Impact Journals LLC

DOI： 10.18632/oncotarget.24570

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L-DOPA sensitizes vasomotor tone by modulating the vascular alpha1-adrenergic receptor. Reviewed International journal

Masukawa D, Koga M, Sezaki A, Nakao Y, Kamikubo Y, Hashimoto T, Okuyama-Oki Y, Aladeokin AC, Nakamura F, Yokoyama U, Wakui H, Ichinose H, Sakurai T, Umemura S, Tamura K, Ishikawa Y, Goshima Y

JCI insight 2 ( 18 ) 2017.9

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Blood pressure is regulated by extrinsic factors including noradrenaline, the sympathetic neurotransmitter that controls cardiovascular functions through adrenergic receptors. However, the fine-tuning system of noradrenaline signaling is relatively unknown. We here show that l-3,4-dihydroxyphenylalanine (L-DOPA), a precursor of catecholamines, sensitizes the vascular adrenergic receptor alpha1 (ADRA1) through activation of L-DOPA receptor GPR143. In WT mice, intravenous infusion of the ADRA1 agonist phenylephrine induced a transient elevation of blood pressure. This response was attenuated in Gpr143 gene-deficient (Gpr143-/y) mice. Specific knockout of Gpr143 in vascular smooth muscle cells (VSMCs) also showed a similar phenotype, indicating that L-DOPA directly modulates ADRA1 signaling in the VSMCs. L-DOPA at nanomolar concentrations alone produced no effect on the VSMCs, but it enhanced phenylephrine-induced vasoconstriction and intracellular Ca2+ responses. Phenylephrine also augmented the phosphorylation of extracellular signal-regulated kinases in cultured VSMCs from WT but not Gpr143-/y mice. In WT mice, blood pressure increased during the transition from light-rest to dark-active phases. This elevation was not observed in Gpr143-/y mice. Taken together, our findings provide evidence for L-DOPA/GPR143 signaling that exerts precursor control of sympathetic neurotransmission through sensitizing vascular ADRA1.

DOI： 10.1172/jci.insight.90903

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Magnetic metal-complex-conducting copolymer core-shell nanoassemblies for a single-drug anticancer platform Reviewed

Jeong-Hwan Kim, Haruki Eguchi, Masanari Umemura, Itaru Sato, Shigeki Yamada, Yujiro Hoshino, Takatsugu Masuda, Ichio Aoki, Kazuo Sakurai, Masahiro Yamamoto, Yoshihiro Ishikawa

NPG ASIA MATERIALS 9 e367-1 - e367-14 2017.3

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DOI： 10.1038/am.2017.29

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Arterial graft with elastic layer structure grown from cells Reviewed

Utako Yokoyama, Yuta Tonooka, Ryoma Koretake, Taisuke Akimoto, Yuki Gonda, Junichi Saito, Masanari Umemura, Takayuki Fujita, Shinya Sakuma, Fumihito Arai, Makoto Kaneko, Yoshihiro Ishikawa

SCIENTIFIC REPORTS 7 ( 1 ) 140 2017.3

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DOI： 10.1038/s41598-017-00237-1

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Hyperthermia and chemotherapy using Fe(Salen) nanoparticles might impact glioblastoma treatment Reviewed

Makoto Ohtake, Masanari Umemura, Itaru Sato, Taisuke Akimoto, Kayoko Oda, Akane Nagasako, Jeong-Hwan Kim, Takayuki Fujita, Utako Yokoyama, Tomohiro Nakayama, Yujiro Hoshino, Mai Ishiba, Susumu Tokura, Masakazu Hara, Tomoya Muramoto, Sotoshi Yamada, Takatsugu Masuda, Ichio Aoki, Yasushi Takemura, Hidetoshi Murata, Haruki Eguchi, Nobutaka Kawahara, Yoshihiro Ishikawa

SCIENTIFIC REPORTS 7 42783 2017.2

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DOI： 10.1038/srep42783

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EP4 Signaling in Smooth Muscle Cells Attracts Inflammatory Immune Responses in the Aorta Invited Reviewed

Ryo Ishiwata, Utako Yokoyama, Yasuhiro Ichikawa, Daisuke Kurotaki, Shota Yasuda, Motohiko Goda, Shinichi Suzuki, Munetaka Masuda, Tomohiko Tamura, Yoshihiro Ishikawa

CIRCULATION 134 ( Suppl 1 ) A13042 2016.11

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Other Link： http://orcid.org/0000-0001-8006-5485
Simultaneous hyperthermia-chemotherapy with controlled drug delivery using single-drug nanoparticles Reviewed

Itaru Sato, Masanari Umemura, Kenji Mitsudo, Hidenobu Fukumura, Jeong-Hwan Kim, Yujiro Hoshino, Hideyuki Nakashima, Mitomu Kioi, Rina Nakakaji, Motohiko Sato, Takayuki Fujita, Utako Yokoyama, Satoshi Okumura, Hisashi Oshiro, Haruki Eguchi, Iwai Tohnai, Yoshihiro Ishikawa

SCIENTIFIC REPORTS 6 24629 2016.4

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DOI： 10.1038/srep24629

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Use of Three-Dimensional Arterial Models To Predict the In Vivo Behavior of Nanoparticles for Drug Delivery Reviewed

Paninee Chetprayoon, Michiya Matsusaki, Utako Yokoyama, Takanori Tejima, Yoshihiro Ishikawa, Mitsuru Akashi

ANGEWANDTE CHEMIE-INTERNATIONAL EDITION 55 ( 14 ) 4461 - 4466 2016.3

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DOI： 10.1002/anie.201509752

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Heterozygous deletion of sarcolipin maintains normal cardiac function. Reviewed

Shimura D, Kusakari Y, Sasano T, Nakashima Y, Nakai G, Jiao Q, Jin M, Yokota T, Ishikawa Y, Nakano A, Goda N, Minamisawa S

American journal of physiology. Heart and circulatory physiology 310 ( 1 ) H92 - 103 2016.1

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DOI： 10.1152/ajpheart.00411.2015

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Epac1 Deficiency Attenuated Vascular Smooth Muscle Cell Migration and Neointimal Formation Reviewed

Yuko Kato, Utako Yokoyama, Chiharu Yanai, Rina Ishige, Daisuke Kurotaki, Masanari Umemura, Takayuki Fujita, Tetsuo Kubota, Satoshi Okumura, Masataka Sata, Tomohiko Tamura, Yoshihiro Ishikawa

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY 35 ( 12 ) 2617 - 2625 2015.12

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DOI： 10.1161/ATVBAHA.115.306534

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A magnetic anti-cancer compound for magnet-guided delivery and magnetic resonance imaging Reviewed

Haruki Eguchi, Masanari Umemura, Reiko Kurotani, Hidenobu Fukumura, Itaru Sato, Jeong-Hwan Kim, Yujiro Hoshino, Jin Lee, Naoyuki Amemiya, Motohiko Sato, Kunio Hirata, David J. Singh, Takatsugu Masuda, Masahiro Yamamoto, Tsutomu Urano, Keiichiro Yoshida, Katsumi Tanigaki, Masaki Yamamoto, Mamoru Sato, Seiichi Inoue, Ichio Aoki, Yoshihiro Ishikawa

SCIENTIFIC REPORTS 5 2015.3

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Deletion of the angiotensin II type 1 receptor-associated protein enhances renal sodium reabsorption and exacerbates angiotensin II-mediated hypertension Reviewed

Masato Ohsawa, Kouichi Tamura, Hiromichi Wakui, Akinobu Maeda, Toru Dejima, Tomohiko Kanaoka, Kengo Azushima, Kazushi Uneda, Yuko Tsurumi-Ikeya, Ryu Kobayashi, Miyuki Matsuda, Shinichi Uchida, Yoshiyuki Toya, Hiroyuki Kobori, Akira Nishiyama, Akio Yamashita, Yoshihiro Ishikawa, Satoshi Umemura

KIDNEY INTERNATIONAL 86 ( 3 ) 570 - 581 2014.9

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DOI： 10.1038/ki.2014.95

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Epac1 increases migration of endothelial cells and melanoma cells via FGF2-mediated paracrine signaling Reviewed

Erdene Baljinnyam, Masanari Umemura, Christine Chuang, Mariana S. De Lorenzo, Mizuka Iwatsubo, Suzie Chen, James S. Goydos, Yoshihiro Ishikawa, John M. Whitelock, Kousaku Iwatsubo

PIGMENT CELL & MELANOMA RESEARCH 27 ( 4 ) 611 - 620 2014.7

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DOI： 10.1111/pcmr.12250

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Epac1-dependent phospholamban phosphorylation mediates the cardiac response to stresses Reviewed

Satoshi Okumura, Takayuki Fujita, Wenqian Cai, Meihua Jin, Iyuki Namekata, Yasumasa Mototani, Huiling Jin, Yoshiki Ohnuki, Yayoi Tsuneoka, Reiko Kurotani, Kenji Suita, Yuko Kawakami, Shogo Hamaguchi, Takaya Abe, Hiroshi Kiyonari, Takashi Tsunematsu, Yunzhe Bai, Sayaka Suzuki, Yuko Hidaka, Masanari Umemura, Yasuhiro Ichikawa, Utako Yokoyama, Motohiko Sato, Fumio Ishikawa, Hiroko Izumi-Nakaseko, Satomi Adachi-Akahane, Hikaru Tanaka, Yoshihiro Ishikawa

JOURNAL OF CLINICAL INVESTIGATION 124 ( 6 ) 2785 - 2801 2014.6

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DOI： 10.1172/JCI64784

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Prostaglandin E-2 Inhibits Elastogenesis in the Ductus Arteriosus via EP4 Signaling Reviewed

Utako Yokoyama, Susumu Minamisawa, Aki Shioda, Ryo Ishiwata, Mei-Hua Jin, Munetaka Masuda, Toshihide Asou, Yukihiko Sugimoto, Hiroki Aoki, Tomoyuki Nakamura, Yoshihiro Ishikawa

CIRCULATION 129 ( 4 ) 487 - 496 2014.1

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DOI： 10.1161/CIRCULATIONAHA.113.004726

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Therapeutic Effect of EP4 Antagonist on Advanced Abdominal Aortic Aneurysm Reviewed

Utako Yokoyama, Ryo Ishiwata, Noriaki Arakawa, Shinichi Suzuki, Munetaka Masuda, Yoshihiro Ishikawa

CIRCULATION 128 ( 22 ) A12641 2013.11

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The Prostanoid EP4 Receptor and Its Signaling Pathway Reviewed

Utako Yokoyama, Kousaku Iwatsubo, Masanari Umemura, Takayuki Fujita, Yoshihiro Ishikawa

PHARMACOLOGICAL REVIEWS 65 ( 3 ) 1010 - 1052 2013.7

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DOI： 10.1124/pr.112.007195

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Adenylyl cyclase type 5 in cardiac disease, metabolism, and aging. Reviewed

Vatner SF, Park M, Yan L, Lee GJ, Lai L, Iwatsubo K, Ishikawa Y, Pessin J, Vatner DE

American journal of physiology. Heart and circulatory physiology 305 H1 - 8 2013.7

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Type 5 Adenylyl Cyclase Increases Oxidative Stress by Transcriptional Regulation of Manganese Superoxide Dismutase via the SIRT1/FoxO3a Pathway Reviewed

Lo Lai, Lin Yan, Shumin Gao, Che-Lin Hu, Hui Ge, Amy Davidow, Misun Park, Claudio Bravo, Kousaku Iwatsubo, Yoshihiro Ishikawa, Johan Auwerx, David A. Sinclair, Stephen F. Vatner, Dorothy E. Vatner

CIRCULATION 127 ( 16 ) 1692 - + 2013.4

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DOI： 10.1161/CIRCULATIONAHA.112.001212

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Targeted drug delivery system and magnetic resonance imaging with intrinsic ferromagnetic nano-particle compound Reviewed

Eguchi, Haruki, Hirata, Kunio, Kurotani, Reiko, Fukumura, Hidenobu, Singh, David J., Yamamoto, Masahiro, Sato, Itaru, Umemura, Masanori, Yamamoto, Masaki, Nagashima, Yoji, Ishikawa, Yoshihiro

Cancer Research 73 ( 8 ) 2013

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DOI： 10.1158/1538-7445.AM2013-5570

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Caveolin gene transfer improves glucose metabolism in diabetic mice Reviewed

Koji Otsu, Yoshiyuki Toya, Jin Oshikawa, Reiko Kurotani, Takuya Yazawa, Motohiko Sato, Utako Yokoyama, Satoshi Umemura, Susumu Minamisawa, Satoshi Okumura, Yoshihiro Ishikawa

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY 298 ( 3 ) C450 - C456 2010.3

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DOI： 10.1152/ajpcell.00077.2009

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Activator of G Protein Signaling 8 (AGS8) Is Required for Hypoxia-induced Apoptosis of Cardiomyocytes ROLE OF G beta gamma AND CONNEXIN 43 (CX43) Reviewed

Motohiko Sato, Qibin Jiao, Takashi Honda, Reiko Kurotani, Eiji Toyota, Satoshi Okumura, Tatsuo Takeya, Susumu Minamisawa, Stephen M. Lanier, Yoshihiro Ishikawa

JOURNAL OF BIOLOGICAL CHEMISTRY 284 ( 45 ) 31431 - 31440 2009.11

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DOI： 10.1074/jbc.M109.014068

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Epac1 Protects Heart From Lipopolysaccharide-induced Cardiac Dysfunction by Inhibiting the Toll-like Receptor 4 Signaling Pathway Reviewed

Satoshi Okumura, Meihua Jin, Yunzhe Bai, Sayaka Suzuki, Xuezhe Xuan, Wenqian Cai, Yuko Hidaka, Reiko Kurotani, Utako Yokoyama, Yoshihiro Ishikawa

CIRCULATION 120 ( 18 ) S841 - S842 2009.11

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Epac increases melanoma cell migration by a heparan sulfate-related mechanism Reviewed

Erdene Baljinnyam, Kousaku Iwatsubo, Reiko Kurotani, Xu Wang, Coskun Ulucan, Mizuka Iwatsubo, David Lagunoff, Yoshihiro Ishikawa

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY 297 ( 4 ) C802 - C813 2009.10

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DOI： 10.1152/ajpcell.00129.2009

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Oxygenation Promotes Smooth Muscle Cell Migration in the Rat Ductus Arteriosus Reviewed

Susumu Minamisawa, Toru Akaike, Utako Yokoyama, Motoi Ozawa, Shiho Iwasaki, Yoshihiro Ishikawa

CIRCULATION RESEARCH 105 ( 7 ) E29 - E29 2009.9

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T-type Ca2+ Channels Promote Oxygenation-induced Closure of the Rat Ductus Arteriosus Not Only by Vasoconstriction but Also by Neointima Formation Reviewed

Toru Akaike, Mei-Hua Jin, Utako Yokoyama, Hiroko Izumi-Nakaseko, Qibin Jiao, Shiho Iwasaki, Mari Iwamoto, Shigeru Nishimaki, Motohiko Sato, Shumpei Yokota, Yoshinori Kamiya, Satomi Adachi-Akahane, Yoshihiro Ishikawa, Susumu Minamisawa

JOURNAL OF BIOLOGICAL CHEMISTRY 284 ( 36 ) 24025 - 24034 2009.9

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DOI： 10.1074/jbc.M109.017061

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Sarcalumenin is essential for maintaining cardiac function during endurance exercise training Reviewed

Qibin Jiao, Yunzhe Bai, Toru Akaike, Hiroshi Takeshima, Yoshihiro Ishikawa, Susumu Minamisawa

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY 297 ( 2 ) H576 - H582 2009.8

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DOI： 10.1152/ajpheart.00946.2008

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Prostaglandin E-2-activated Epac promotes neointimal formation of the rat ductus arteriosus by a process distinct from that of cAMP-dependent protein kinase A Reviewed

Utako Yokoyama, Susumu Minamisawa, Hong Quan, Toru Akaike, Sayaka Suzuki, Meihua Jin, Qibin Jiao, Mayumi Watanabe, Koji Otsu, Shiho Iwasaki, Shigeru Nishimaki, Motohiko Sato, Yoshihiro Ishikawa

JOURNAL OF BIOLOGICAL CHEMISTRY 283 ( 42 ) 28702 - 28709 2008.10

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DOI： 10.1074/jbc.M804223200

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Epac1 is upregulated during neointima formation and promotes vascular smooth muscle cell migration Reviewed

Utako Yokoyama, Susumu Minamisawa, Hong Quan, Toru Akaike, Meihua Jin, Koji Otsu, Coskun Ulucan, Xu Wang, Erdenechimeg Baljinnyam, Minoru Takaoka, Masataka Sata, Yoshihiro Ishikawa

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY 295 ( 4 ) H1547 - H1555 2008.10

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DOI： 10.1152/ajpheart.01317.2007

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Type 5 adenylyl cyclase plays a major role in stabilizing heart rate in response to microgravity induced by parabolic flight Reviewed

Satoshi Okumura, Takashi Tsunematsu, Yunzhe Bai, Qibin Jiao, Shinji Ono, Sayaka Suzuki, Reiko Kurotani, Motohiko Sato, Susumu Minamisawa, Satoshi Umemura, Yoshihiro Ishikawa

JOURNAL OF APPLIED PHYSIOLOGY 105 ( 1 ) 173 - 179 2008.7

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DOI： 10.1152/japplphysiol.01166.2007

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Sarcalumenin alleviates stress-induced cardiac dysfunction by improving Ca2+ handling of the sarcoplasmic reticulum Reviewed

Miei Shimura, Susumu Minamisawa, Hiroshi Takeshima, Qibin Jiao, Yunzhe Bai, Satoshi Umemura, Yoshihiro Ishikawa

CARDIOVASCULAR RESEARCH 77 ( 2 ) 362 - 370 2008.1

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DOI： 10.1093/cvr/cvm019

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Disruption of type 5 adenylyl cyclase enhances desensitization of cyclic adenosine monophosphate signal and increases Akt signal with chronic catecholamine stress Reviewed

Satoshi Okumura, Dorothy E. Vatner, Reiko Kurotani, Yunzhe Bai, Shumin Gao, Zengrong Yuan, Kousaku Iwatsubo, Coskun Ulucan, Jun-ichi Kawabe, Kaushik Ghosh, Stephen F. Vatner, Yoshihlro Ishikawa

CIRCULATION 116 ( 16 ) 1776 - 1783 2007.10

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DOI： 10.1161/CIRCULATIONAHA.107.698662

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cAMP-dependent intimal cushion formation of the rat ductus arteriosus: The role of Epac Reviewed

Hong Quan, Utako Yokoyama, Mayumi Watanabe, Toru Akaike, Koji Otsu, Shiho Iwasaki, Yoshihiro Ishikawa, Susumu Minamisawa

CIRCULATION 116 ( 16 ) 110 - 110 2007.10

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Epac 1 is upregulated after mechanical vascular injury and promotes smooth muscle cell migration Reviewed

Utako Yokoyama, Susumu Minamisawa, Coskun Ulcan, Xu Wang, Minoru Takaoka, Quan Hong, Koji Otsu, Masataka Sata, Yoshihiro Ishikawa

CIRCULATION 114 ( 18 ) 230 - 230 2006.10

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Multiple transcripts of Ca2+ channel alpha(1)-subunits and a novel spliced variant of the alpha(1C)-subunit in rat ductus arteriosus Reviewed

U Yokoyama, S Minamisawa, S Adachi-Akahane, T Akaike, Naguro, I, K Funakoshi, M Iwamoto, M Nakagome, N Uemura, H Hori, S Yokota, Y Ishikawa

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY 290 ( 4 ) H1660 - H1670 2006.4

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DOI： 10.1152/ajpheart.00100.2004

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Direct inhibition of type 5 adenylyl cyclase prevents myocardial apoptosis without functional deterioration Reviewed

K Iwatsubo, S Minamisawa, T Tsunematsu, M Nakagome, Y Toya, JE Tomlinson, S Umemura, RM Scarborough, DE Levy, Y Ishikawa

JOURNAL OF BIOLOGICAL CHEMISTRY 279 ( 39 ) 40938 - 40945 2004.9

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DOI： 10.1074/jbc.M314238200

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Nicotinic acetylcholine receptor alpha(7) regulates cAMP signal within lipid rafts Reviewed

J Oshikawa, Y Toya, T Fujita, M Egawa, J Kawabe, S Umemura, Y Ishikawa

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY 285 ( 3 ) C567 - C574 2003.9

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DOI： 10.1152/ajpcell.00422.2002

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Type 5 adenylyl cyclase disruption alters not only sympathetic but also parasympathetic and calcium-mediated cardiac regulation. Reviewed

Okumura Satoshi, Kawabe Jun-ichi, Yatani Atsuko, Takagi Gen, Lee Ming-Chih, Hong Chull, Liu Jing, Takagi Ikuyo, Sadoshima Junichi, Vatner Dorothy E, Vatner, Stephen F, Ishikawa Yoshihiro

Circulation Research 93 ( 4 ) 364 - 71 2003.8

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DOI： 10.1161/01.RES.0000086986.35568.63

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Disruption of type 5 adenylyl cyclase gene preserves cardiac function against pressure overload Reviewed

S Okumura, G Takagi, J Kawabe, GP Yang, MC Lee, C Hong, J Liu, DE Vatner, J Sadoshima, SF Vatner, Y Ishikawa

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 100 ( 17 ) 9986 - 9990 2003.8

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DOI： 10.1073/pnas.1733772100

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Type 5 adenylyl cyclase disruption alters not only sympathetic but also parasympathetic and calcium-mediated cardiac regulation Reviewed

S Okumura, J Kawabe, A Yatani, G Takagi, MC Lee, C Hong, J Liu, Takagi, I, J Sadoshima, DE Vatner, SF Vatner, Y Ishikawa

CIRCULATION RESEARCH 93 ( 4 ) 364 - 371 2003.8

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In a genetically engineered mouse line with disruption of type 5 adenylyl cyclase (AC5(-/-)), a major cardiac isoform, there was no compensatory increase in other isoforms of AC in the heart. Both basal and isoproterenol (ISO)-stimulated AC activities were decreased by 30% to 40% in cardiac membranes. The reduced AC activity did not affect cardiac function (left ventricular ejection fraction [LVEF]) at baseline. However, increases in LVEF after ISO were significantly attenuated in AC5(-/-) (P<0.05, n=11). Paradoxically, conscious AC5(-/)- mice had a higher heart rate compared with wild-type (WT) mice (613&PLUSMN;8 versus 523&PLUSMN;11 bpm, P<0.01, n=14 to 15). Muscarinic agonists decreased AC activity, LVEF, and heart rate more in WT than in AC5(-/-). In addition, baroreflex-mediated, ie, neuronally regulated, bradycardia after phenylephrine was also attenuated in AC5(-/-). The carbachol-activated outward potassium current (at -40 mV) normalized to cell capacitance in AC5(-/-) (2.6+/-0.4 pA/pF, n=16) was similar to WT (2.9+/-0.3 pA/pF, n=27), but calcium (Ca2+)-mediated inhibition of AC activity and Ca2+ channel function were diminished in AC5(-/-). Thus, AC5(-/-) attenuates sympathetic responsiveness and also impairs parasympathetic and Ca2+-mediated regulation of the heart, indicating that those actions are not only regulated at the level of the receptor and G-protein but also at the level of type 5 AC.

DOI： 10.1161/01.RES.0000086986.35568.63

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Motor dysfunction in type 5 adenylyl cyclase-null mice Reviewed

T Iwamoto, S Okumura, K Iwatsubo, JI Kawabe, K Ohtsu, Sakai, I, Y Hashimoto, A Izumitani, K Sango, K Ajiki, Y Toya, S Umemura, Y Goshima, N Arai, SF Vatner, Y Ishikawa

JOURNAL OF BIOLOGICAL CHEMISTRY 278 ( 19 ) 16936 - 16940 2003.5

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DOI： 10.1074/jbc.C300075200

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Atrial chamber-specific expression of sarcolipin is regulated during development and hypertrophic remodeling Reviewed

S Minamisawa, YB Wang, J Chen, Y Ishikawa, KR Chien, R Matsuoka

JOURNAL OF BIOLOGICAL CHEMISTRY 278 ( 11 ) 9570 - 9575 2003.3

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DOI： 10.1074/jbc.M213132200

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Type-specific regulation of adenylyl cyclase. Selective pharmacological stimulation and inhibition of adenylyl cyclase isoforms. Reviewed

T Onda, Y Hashimoto, M Nagai, H Kuramochi, S Saito, H Yamazaki, Y Toya, Sakai, I, CJ Homcy, K Nishikawa, Y Ishikawa

JOURNAL OF BIOLOGICAL CHEMISTRY 276 ( 51 ) 47785 - 47793 2001.12

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DOI： 10.1074/jbc.M107233200

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Accumulation of molecules involved in alpha 1-adrenergic signal within caveolae: caveolin expression and the development of cardiac hypertrophy Reviewed

T Fujita, Y Toya, K Iwatsubo, T Onda, K Kimura, S Umemura, Y Ishikawa

CARDIOVASCULAR RESEARCH 51 ( 4 ) 709 - 716 2001.9

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Determinants of the Cardiomyopathic Phenotype in Chimeric Mice Overexpressing Cardiac Gsα

Dorothy E. Vatner, Gui-Ping Yang, Yong-Jian Geng, Kuniya Asai, Jeung S. Yun, Thomas E. Wagner, Yoshihiro Ishikawa, Sanford P. Bishop, Charles J. Homcy, Stephen F. Vatner

Circulation Research 86 ( 7 ) 802 - 806 2000.4

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DOI： 10.1161/01.res.86.7.802

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beta-Adrenergic receptor blockade arrests myocyte damage and preserves cardiac function in the transgenic G(s alpha) mouse Reviewed

K Asai, GP Yang, YJ Geng, G Takagi, S Bishop, Y Ishikawa, RP Shannon, TE Wagner, DE Vatner, CJ Homcy, SF Vatner

JOURNAL OF CLINICAL INVESTIGATION 104 ( 5 ) 551 - 558 1999.9

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Compartmentation of cyclic adenosine 3 ',5 '-monophosphate signaling in caveolae Reviewed

C Schwencke, M Yamamoto, S Okumura, Y Toya, SJ Kim, Y Ishikawa

MOLECULAR ENDOCRINOLOGY 13 ( 7 ) 1061 - 1070 1999.7

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Beta-adrenergic receptor– G protein–adenylyl cyclase signal transduction in the failing heart

Dorothy E Vatner, Kuniya Asai, Mitsunori Iwase, Yoshihiro Ishikawa, Richard P Shannon, Charles J Homcy, Stephen F Vatner

The American Journal of Cardiology 83 ( 12 ) 80 - 85 1999.6

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DOI： 10.1016/s0002-9149(99)00266-0

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Mechanisms of desensitization to a PDE inhibitor (milrinone) in conscious dogs with heart failure. Reviewed

Sato N, Asai K, Okumura S, Takagi G, Shannon R P, Fujita-Yamaguchi Y, Ishikawa Y, Vatner S F, Vatner D E

The American Journal of Physiology 276 ( 5 ) H1699 - 705 1999.5

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DOI： 10.1152/ajpheart.1999.276.5.H1699

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Mechanisms of desensitization to a PDE inhibitor (milrinone) in conscious dogs with heart failure Reviewed

N Sato, K Asai, S Okumura, G Takagi, RP Shannon, Y Fujita-Yamaguchi, Y Ishikawa, SF Vatner, DE Vatner

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY 276 ( 5 ) H1699 - H1705 1999.5

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Differential regulation of inotropy and lusitropy in overexpressed Gsα myocytes through cAMP and Ca2+ channel pathways

Song-Jung Kim, Atsuko Yatani, Dorothy E. Vatner, Satoshi Yamamoto, Yoshihiro Ishikawa, Thomas E. Wagner, Richard P. Shannon, Young-Kwon Kim, Gen Takagi, Kuniya Asai, Charles J. Homcy, Stephen F. Vatner

Journal of Clinical Investigation 103 ( 7 ) 1089 - 1097 1999.4

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DOI： 10.1172/jci4848

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Overexpression of myocardial Gsalpha prevents full expression of catecholamine desensitization despite increased beta-adrenergic receptor kinase. Reviewed

D E Vatner, K Asai, M Iwase, Y Ishikawa, T E Wagner, R P Shannon, C J Homcy, S F Vatner

Journal of Clinical Investigation 101 ( 9 ) 1916 - 1922 1998.5

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DOI： 10.1172/jci1530

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Inhibition of adenylyl cyclase by caveolin peptides Reviewed

Y Toya, C Schwencke, J Couet, MP Lisanti, Y Ishikawa

ENDOCRINOLOGY 139 ( 4 ) 2025 - 2031 1998.4

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Depressed Heart Rate Variability and Arterial Baroreflex in Conscious Transgenic Mice With Overexpression of Cardiac G sα

Masami Uechi, Kuniya Asai, Motohisa Osaka, Amelia Smith, Naoki Sato, Thomas E. Wagner, Yoshihiro Ishikawa, Hirokazu Hayakawa, Dorothy E. Vatner, Richard P. Shannon, Charles J. Homcy, Stephen F. Vatner

Circulation Research 82 ( 4 ) 416 - 423 1998.3

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DOI： 10.1161/01.res.82.4.416

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Downregulation of caveolin by chronic beta-adrenergic receptor stimulation in mice Reviewed

N Oka, K Asai, RK Kudej, JG Edwards, Y Toya, C Schwencke, DE Vatner, SF Vatner, Y Ishikawa

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY 273 ( 6 ) C1957 - C1962 1997.12

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Caveolin interaction with protein kinase C - Isoenzyme-dependent regulation of kinase activity by the caveolin scaffolding domain peptide Reviewed

N Oka, M Yamamoto, C Schwencke, J Kawabe, T Ebina, S Ohno, J Couet, MP Lisanti, Y Ishikawa

JOURNAL OF BIOLOGICAL CHEMISTRY 272 ( 52 ) 33416 - 33421 1997.12

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Cardiomyopathy induced by cardiac Gs alpha overexpression Reviewed

M. Iwase, M. Uechi, D. E. Vatner, K. Asai, R. P. Shannon, R. K. Kudej, T. E. Wagner, D. C. Wight, T. A. Patrick, Y. Ishikawa, C. J. Homcy, S. F. Vatner

American Journal of Physiology-Heart and Circulatory Physiology 272 ( 1 ) H585 - H589 1997.1

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The goal of this study was to determine whether chronic endogenous sympathetic stimulation resulting from the overexpression of cardiac stimulatory G protein alpha subunit (Gs alpha) in transgenic mice (15.3 +/- 0.1 mo old) resulted in a clinical picture of cardiomyopathy. The left ventricular ejection fraction, measured by echocardiography, was reduced in older mice with Gs alpha overexpression (50.4 +/- 5.4%) compared with age-matched control mice (70.9 +/- 1.6%; P < 0.05). When ejection fractions were compared at similar heart rates, the Gs alpha mice exhibited a greater left ventricular end-diastolic dimension than control mice (4.3 +/- 0.2 vs. 3.7 +/- 0.1 mm; P < 0.05). Baseline heart rates were elevated in conscious Gs alpha mice (722 +/- 27 beats/min; n = 5) compared with control mice (656 +/- 28 beats/min; n = 5). Moreover, electrocardiographic monitoring demonstrated a high incidence of arrhythmias. Increased mortality compared with control mice (31.6 vs. 3.0%; P< 0.01) was also observed. Thus older mice with Gs alpha overexpression exhibit many of the features of dilated cardiomyopathy. This study supports the concept that chronic sympathetic stimulation over an extended period of time, i.e., over the life of an animal, is deleterious and actually may result in cardiomyopathy.

DOI： 10.1152/ajpheart.1997.272.1.h585

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Soluble adenylyl cyclase from Spodoptera frugiperda (Sf9) cells - Purification and biochemical characterization Reviewed

J Kawabe, Y Toya, C Schwencke, N Oka, T Ebina, Y Ishikawa

JOURNAL OF BIOLOGICAL CHEMISTRY 271 ( 33 ) 20132 - 20137 1996.8

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REGULATION OF ADENYLYL-CYCLASE BY PROTEIN-KINASE-A Reviewed

G IWAMI, J KAWABE, T EBINA, PJ CANNON, CJ HOMCY, Y ISHIKAWA

JOURNAL OF BIOLOGICAL CHEMISTRY 270 ( 21 ) 12481 - 12484 1995.5

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DIFFERENTIAL ACTIVATION OF ADENYLYL-CYCLASE BY PROTEIN-KINASE-C ISOENZYMES Reviewed

J KAWABE, G IWAMI, T EBINA, S OHNO, T KATADA, Y UEDA, CJ HOMCY, Y ISHIKAWA

JOURNAL OF BIOLOGICAL CHEMISTRY 269 ( 24 ) 16554 - 16558 1994.6

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DOWN-REGULATION OF ADENYLYLCYCLASE TYPE-V AND TYPE-VI MESSENGER-RNA LEVELS IN PACING-INDUCED HEART-FAILURE IN DOGS Reviewed

Y ISHIKAWA, S SOROTA, K KIUCHI, RP SHANNON, K KOMAMURA, S KATSUSHIKA, DE VATNER, SF VATNER, CJ HOMCY

JOURNAL OF CLINICAL INVESTIGATION 93 ( 5 ) 2224 - 2229 1994.5

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DOI： 10.1172/JCI117219

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CLONING AND CHARACTERIZATION OF A 6TH ADENYLYL CYCLASE ISOFORM - TYPE-V AND TYPE-VI CONSTITUTE A SUBGROUP WITHIN THE MAMMALIAN ADENYLYL CYCLASE FAMILY Reviewed

S KATSUSHIKA, L CHEN, JI KAWABE, R NILAKANTAN, NJ HALNON, CJ HOMCY, Y ISHIKAWA

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 89 ( 18 ) 8774 - 8778 1992.9

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ISOLATION AND CHARACTERIZATION OF A NOVEL CARDIAC ADENYLYLCYCLASE CDNA Reviewed

Y ISHIKAWA, S KATSUSHIKA, L CHEN, NJ HALNON, J KAWABE, CJ HOMCY

JOURNAL OF BIOLOGICAL CHEMISTRY 267 ( 19 ) 13553 - 13557 1992.7

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Translationally controlled tumor protein interacts with connexin 43 and facilitates intercellular coupling between cardiomyocytes

Yaopeng Hu, Wenqian Cai, Yuko Hidaka, Keizo Hiraishi, Jiehui Cang, Masanari Umemura, Utako Yokoyama, Björn C. Knollmann, Yoshihiro Ishikawa, Takayuki Fujita

Frontiers in Cell and Developmental Biology 13 2025.3

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Introduction

Connexins are gap junction proteins that play pivotal roles in intercellular communication. Connexin 43 (Cx43) is one of the most ubiquitously expressed connexin isoforms in human. Cx43 has been demonstrated to be involved in the pathological process of various diseases, including arrhythmias. Recently, translationally controlled tumor protein (TCTP), a highly conserved anti-apoptotic protein, has been shown to play an important role in protecting against the development of heart failure. However, its role in arrhythmogenesis remains unclear. In this study, we aimed to examine the interaction between TCTP and Cx43 and investigate the roles of TCTP in the formation of Cx43 gap junction channels and gap junctional intercellular communication (GJIC) in cardiomyocytes.

Methods and results

We found that TCTP was predominantly expressed in the intercalated discs of mouse heart tissue. Cx43 in adult mouse hearts was coimmunoprecipitated using a TCTP-specific antibody. Additionally, co-localization of TCTP and Cx43 was demonstrated using a proximity ligation assay in iPS cell-derived human cardiomyocytes. TCTP silencing reduced the formation of Cx43 gap junction channels at the intercellular contacts between cardiomyocytes. Moreover, TCTP silencing significantly attenuated GJIC among cardiomyocytes. Interestingly, the development of ventricular arrhythmia was attenuated in cardiomyocyte-specific TCTP-overexpressing mice.

Conclusion

These findings indicate that TCTP regulates GJIC. Thus, TCTP may be a therapeutic target for preventing Cx43-related pathogenesis.

DOI： 10.3389/fcell.2025.1549063

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Cytotoxic effects of the cigarette smoke extract of heated tobacco products on human oral squamous cell carcinoma: the role of reactive oxygen species and CaMKK2.

Nagao Kagemichi, Masanari Umemura, Soichiro Ishikawa, Yu Iida, Shota Takayasu, Akane Nagasako, Rina Nakakaji, Taisuke Akimoto, Makoto Ohtake, Takahiro Horinouchi, Tetsuya Yamamoto, Yoshihiro Ishikawa

The journal of physiological sciences : JPS 74 ( 1 ) 35 - 35 2024.6

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BACKGROUND: The increasing prevalence of heated tobacco products (HTPs) has heightened concerns regarding their potential health risks. Previous studies have demonstrated the toxicity of cigarette smoke extract (CSE) from traditional tobacco's mainstream smoke, even after the removal of nicotine and tar. Our study aimed to investigate the cytotoxicity of CSE derived from HTPs and traditional tobacco, with a particular focus on the role of reactive oxygen species (ROS) and intracellular Ca2+. METHODS: A human oral squamous cell carcinoma (OSCC) cell line, HSC-3 was utilized. To prepare CSE, aerosols from HTPs (IQOS) and traditional tobacco products (1R6F reference cigarette) were collected into cell culture media. A cell viability assay, apoptosis assay, western blotting, and Fluo-4 assay were conducted. Changes in ROS levels were measured using electron spin resonance spectroscopy and the high-sensitivity 2',7'-dichlorofluorescein diacetate assay. We performed a knockdown of calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2) by shRNA lentivirus in OSCC cells. RESULTS: CSE from both HTPs and traditional tobacco exhibited cytotoxic effects in OSCC cells. Exposure to CSE from both sources led to an increase in intracellular Ca2+ concentration and induced p38 phosphorylation. Additionally, these extracts prompted cell apoptosis and heightened ROS levels. N-acetylcysteine (NAC) mitigated the cytotoxic effects and p38 phosphorylation. Furthermore, the knockdown of CaMKK2 in HSC-3 cells reduced cytotoxicity, ROS production, and p38 phosphorylation in response to CSE. CONCLUSION: Our findings suggest that the CSE from both HTPs and traditional tobacco induce cytotoxicity. This toxicity is mediated by ROS, which are regulated through Ca2+ signaling and CaMKK2 pathways.

DOI： 10.1186/s12576-024-00928-1

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Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming

Taisuke Akimoto, Md Rafikul Islam, Akane Nagasako, Kazuhito Kishi, Rina Nakakaji, Makoto Ohtake, Hisashi Hasumi, Takashi Yamaguchi, Shigeki Yamada, Tetsuya Yamamoto, Yoshihiro Ishikawa, Masanari Umemura

Cancer Science 2024.6

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Abstract

Application of physical forces, ranging from ultrasound to electric fields, is recommended in various clinical practice guidelines, including those for treating cancers and bone fractures. However, the mechanistic details of such treatments are often inadequately understood, primarily due to the absence of comprehensive study models. In this study, we demonstrate that an alternating magnetic field (AMF) inherently possesses a direct anti‐cancer effect by enhancing oxidative phosphorylation (OXPHOS) and thereby inducing metabolic reprogramming. We observed that the proliferation of human glioblastoma multiforme (GBM) cells (U87 and LN229) was inhibited upon exposure to AMF within a specific narrow frequency range, including around 227 kHz. In contrast, this exposure did not affect normal human astrocytes (NHA). Additionally, in mouse models implanted with human GBM cells in the brain, daily exposure to AMF for 30 min over 21 days significantly suppressed tumor growth and prolonged overall survival. This effect was associated with heightened reactive oxygen species (ROS) production and increased manganese superoxide dismutase (MnSOD) expression. The anti‐cancer efficacy of AMF was diminished by either a mitochondrial complex IV inhibitor or a ROS scavenger. Along with these observations, there was a decrease in the extracellular acidification rate (ECAR) and an increase in the oxygen consumption rate (OCR). This suggests that AMF‐induced metabolic reprogramming occurs in GBM cells but not in normal cells. Our results suggest that AMF exposure may offer a straightforward strategy to inhibit cancer cell growth by leveraging oxidative stress through metabolic reprogramming.

DOI： 10.1111/cas.16243

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EP4-induced mitochondrial localization and cell migration mediated by CALML6 in human oral squamous cell carcinoma

Soichiro Ishikawa, Masanari Umemura, Rina Nakakaji, Akane Nagasako, Kagemichi Nagao, Yuto Mizuno, Kei Sugiura, Mitomu Kioi, Kenji Mitsudo, Yoshihiro Ishikawa

Communications Biology 7 ( 1 ) 2024.5

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Publishing type：Research paper (scientific journal) Publisher：Springer Science and Business Media LLC

Abstract

Lymph node metastasis, primarily caused by the migration of oral squamous cell carcinoma (OSCC) cells, stands as a crucial prognostic marker. We have previously demonstrated that EP4, a subtype of the prostaglandin E2 (PGE2) receptor, orchestrates OSCC cell migration via Ca2+ signaling. The exact mechanisms by which EP4 influences cell migration through Ca2+ signaling, however, is unclear. Our study aims to clarify how EP4 controls OSCC cell migration through this pathway. We find that activating EP4 with an agonist (ONO-AE1-473) increased intracellular Ca2+ levels and the migration of human oral cancer cells (HSC-3), but not human gingival fibroblasts (HGnF). Further RNA sequencing linked EP4 to calmodulin-like protein 6 (CALML6), whose role remains undefined in OSCC. Through protein-protein interaction network analysis, a strong connection is identified between CALML6 and calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2), with EP4 activation also boosting mitochondrial function. Overexpressing EP4 in HSC-3 cells increases experimental lung metastasis in mice, whereas inhibiting CaMKK2 with STO-609 markedly lowers these metastases. This positions CaMKK2 as a potential new target for treating OSCC metastasis. Our findings highlight CALML6 as a pivotal regulator in EP4-driven mitochondrial respiration, affecting cell migration and metastasis via the CaMKK2 pathway.

DOI： 10.1038/s42003-024-06231-4

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Other Link： https://www.nature.com/articles/s42003-024-06231-4
Hydrostatic pressure under hypoxia facilitates fabrication of tissue-engineered vascular grafts derived from human vascular smooth muscle cells in vitro. International journal

Tomoyuki Kojima, Takashi Nakamura, Junichi Saito, Yuko Hidaka, Taisuke Akimoto, Hana Inoue, Christian Nanga Chick, Toyonobu Usuki, Makoto Kaneko, Etsuko Miyagi, Yoshihiro Ishikawa, Utako Yokoyama

Acta biomaterialia 171 209 - 222 2023.10

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Biologically compatible vascular grafts are urgently required. The scaffoldless multi-layered vascular wall is considered to offer theoretical advantages, such as facilitating cells to form cell-cell and cell-matrix junctions and natural extracellular matrix networks. Simple methods are desired for fabricating physiological scaffoldless tissue-engineered vascular grafts. Here, we showed that periodic hydrostatic pressurization under hypoxia (HP/HYP) facilitated the fabrication of multi-layered tunica media entirely from human vascular smooth muscle cells. Compared with normoxic atmospheric pressure, HP/HYP increased expression of N-myc downstream-regulated 1 (NDRG1) and the collagen-cross-linking enzyme lysyl oxidase in human umbilical artery smooth muscle cells. HP/HYP increased N-cadherin-mediated cell-cell adhesion via NDRG1, cell-matrix interaction (i.e., clustering of integrin α5β1 and fibronectin), and collagen fibrils. We then fabricated vascular grafts using HP/HYP during repeated cell seeding and obtained 10-layered smooth muscle grafts with tensile rupture strength of 0.218-0.396 MPa within 5 weeks. Implanted grafts into the rat aorta were endothelialized after 1 week and patent after 5 months, at which time most implanted cells had been replaced by recipient-derived cells. These results suggest that HP/HYP enables fabrication of scaffoldless human vascular mimetics that have a spatial arrangement of cells and matrices, providing potential clinical applications for cardiovascular diseases. STATEMENT OF SIGNIFICANCE: Tissue-engineered vascular grafts (TEVGs) are theoretically more biocompatible than prosthetic materials in terms of mechanical properties and recipient cell-mediated tissue reconstruction. Although some promising results have been shown, TEVG fabrication processes are complex, and the ideal method is still desired. We focused on the environment in which the vessels develop in utero and found that mechanical loading combined with hypoxia facilitated formation of cell-cell and cell-matrix junctions and natural extracellular matrix networks in vitro, which resulted in the fabrication of multi-layered tunica media entirely from human umbilical artery smooth muscle cells. These scaffoldless TEVGs, produced using a simple process, were implantable and have potential clinical applications for cardiovascular diseases.

DOI： 10.1016/j.actbio.2023.09.041

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Physiological Functions of Calcium Signaling via Orai1 in Various Cancers Invited Reviewed

Umemura M, Nakakaji R, Ishikawa Y

The Journal of Physiological Sciences (100周年記念号) 73 ( 21 ) 2023.9

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DOI： 10.1186/s12576-023-00878-0

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口腔がん細胞におけるEP4受容体のミトコンドリア生合成を介した遊走調節機構の解明

石川聡一郎, 梅村将就, 中鍛治里奈, 永迫茜, 大澤昂平, 深江和奏, 山下絵利子, 光藤健司, 石川義弘

日本病態生理学会雑誌 32 ( 2 ) 40 - 40 2023.7

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低酸素下加圧培養によるヒト臍帯動脈平滑筋細胞由来の人工血管の作製

小嶋朋之, 齋藤純一, 中村隆, 井上華, 石川義弘, 横山詩子

日本小児循環器学会総会・学術集会抄録集 58回 [III - 02] 2022.7

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口腔がん細胞遊走におけるEP4受容体のCa2+シグナルを介したメカニズムの解明

石川聡一郎, 梅村将就, 中鍛治里奈, 永迫茜, 大澤昂平, 來生知, 光藤健司, 石川義弘

日本病態生理学会雑誌 31 ( 2 ) 23 - 23 2022.7

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Methotrexate-Transferrin-Functionalized Fe(Salen)-Polypyrrole Nanocomposites for Targeted Photo-/Magneto-Thermal Cancer Treatments Reviewed

Journal of Composites Science 6 ( 5 ) 2022.5

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DOI： 10.3390/jcs6050136

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Store-operated calcium entry via ORAI1 regulates doxorubicin-induced apoptosis and prevents cardiotoxicity in cardiac fibroblasts. International journal

Hiroko Nemoto, Masanari Umemura, Fumina Suzuki, Akane Nagasako, Kagemichi Nagao, Yuko Hidaka, Rina Nakakaji, Keiji Uchida, Shinichi Suzuki, Munetaka Masuda, Yoshihiro Ishikawa

PloS one 17 ( 12 ) e0278613 2022

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Despite exhibiting cardiotoxicity, doxorubicin (DOX) is widely used for cancer treatments. Cardiac fibroblasts (CFs) are important in the pathogenesis of heart failure. This necessitates the study of the effect of DOX on CFs. The impairment of calcium (Ca2+) homeostasis is a common mechanism of heart failure. Store-operated Ca2+ entry (SOCE) is a receptor-regulated Ca2⁺ entry pathway that maintains calcium balance by sensing reduced calcium stores in the endoplasmic reticulum. ORAI1, a calcium channel protein and the most important component of SOCE, is highly expressed in human cardiac fibroblasts (HCFs). It is upregulated in CFs from failing ventricles. However, whether ORAI1 in HCFs is increased and/or plays a role in DOX-induced cardiotoxicity remains unknown. In this study, we aimed to elucidate the relationship between ORAI1/SOCE and DOX-induced heart failure. Induction of apoptosis by DOX was characterized in HCFs. Apoptosis and cell cycle analyses were performed by fluorescence-activated cell sorting (FACS). Reactive oxygen species (ROS) production was measured using fluorescence. YM-58483 was used as an ORAI1/SOCE inhibitor. ORAI1-knockdown cells were established by RNA interference. In vivo experiments were performed by intraperitoneally injecting YM-58483 and DOX into mice. We first demonstrated that DOX significantly increased the protein expression level of p53 in HCFs by western blotting. FACS analysis revealed that DOX increased early apoptosis and induced cell cycle arrest in the G2 phase in fibroblasts. DOX also increased ROS production. DOX significantly increased the expression level of ORAI1 in CFs. Both YM-58483 and ORAI1 gene knockdown attenuated DOX-induced apoptosis. Similarly, YM-58483 attenuated cell cycle arrest in the G2 phase, and ORAI1 knockdown attenuated DOX-induced ROS production in HCFs. In the animal experiment, YM-58483 attenuated DOX-induced apoptosis. In HCFs, ORAI1/SOCE regulates p53 expression and plays an important role in DOX-induced cardiotoxicity. ORAI1 may serve as a new target for preventing DOX-induced heart failure.

DOI： 10.1371/journal.pone.0278613

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心臓線維芽細胞におけるOrai1を介したドキソルビシン関連心不全の新たな機序

根本寛子, 梅村将就, 中鍛治里奈, 永迫茜, 長尾景充, 日高祐子, Islam Rafikul, 鈴木文菜, 鈴木伸一, 石川義弘

日本病態生理学会雑誌 30 ( 2 ) 36 - 36 2021.12

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ラット心臓横紋筋におけるドキソルビシンの心毒性メカニズムの解析

鈴木文菜, 梅村将就, 内野萌, 根本寛子, 日高祐子, 永迫茜, 中鍛治里奈, 石川義弘

日本病態生理学会雑誌 30 ( 2 ) 41 - 41 2021.12

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市販医薬品の薬効成分を磁性化する画期的技術の開発

梅村将就, 中鍛治里奈, 永迫茜, Islam Md Rafikul, 大竹誠, 長尾景充, 根本寛子, 水野雄斗, 石川聡一郎, 鈴木文菜, 石川義弘

横浜医学 72 ( 4 ) 537 - 544 2021.10

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市販医薬品の薬効成分を磁性化する画期的技術の開発

梅村将就, 中鍛治里奈, 永迫茜, Islam Md Rafikul, 大竹誠, 長尾景充, 根本寛子, 水野雄斗, 石川聡一郎, 鈴木文菜, 石川義弘

横浜医学 72 ( 4 ) 537 - 544 2021.10

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Increased Plasma Levels of Myosin Heavy Chain 11 Is Associated with Atherosclerosis. International journal

Lisa Takahashi, Tomoaki Ishigami, Hirofumi Tomiyama, Yuko Kato, Hiroyuki Kikuchi, Koichiro Tasaki, Jun Yamashita, Shigeru Inoue, Masataka Taguri, Toshitaka Nagao, Taishiro Chikamori, Yoshihiro Ishikawa, Utako Yokoyama

Journal of clinical medicine 10 ( 14 ) 2021.7

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Many studies have revealed numerous potential biomarkers for atherosclerosis, but tissue-specific biomarkers are still needed. Recent lineage-tracing studies revealed that smooth muscle cells (SMCs) contribute substantially to plaque formation, and the loss of SMCs causes plaque vulnerability. We investigated the association of SMC-specific myosin heavy chain 11 (myosin-11) with atherosclerosis. Forty-five patients with atherosclerosis and 34 control subjects were recruited into our study. In the atherosclerosis patients, 35 patients had either coronary artery disease (CAD) or peripheral artery disease (PAD), and 10 had both CAD and PAD. Coronary arteries isolated from five patients were subjected to histological study. Circulating myosin-11 levels were higher in the CAD or PAD group than in controls. The area under the receiver operating characteristic curve of myosin-11 was 0.954. Circulating myosin-11 levels in the CAD and PAD group were higher than in the CAD or PAD group, while high-sensitivity C-reactive protein concentrations did not differ between these groups. Multinomial logistic regression analyses showed a significant association of myosin-11 levels with the presence of multiple atherosclerotic regions. Myosin-11 was expressed in the medial layer of human atherosclerotic lesions where apoptosis elevated. Circulating myosin-11 levels may be useful for detecting spatial expansion of atherosclerotic regions.

DOI： 10.3390/jcm10143155

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Challenges and Possibilities of Cell-Based Tissue-Engineered Vascular Grafts

Junichi Saito, Makoto Kaneko, Yoshihiro Ishikawa, Utako Yokoyama

Cyborg and Bionic Systems 2021 1 - 16 2021.2

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Publishing type：Research paper (scientific journal) Publisher：American Association for the Advancement of Science (AAAS)

There is urgent demand for biologically compatible vascular grafts for both adult and pediatric patients. The utility of conventional nonbiodegradable materials is limited because of their thrombogenicity and inability to grow, while autologous vascular grafts involve considerable disadvantages, including the invasive procedures required to obtain these healthy vessels from patients and insufficient availability in patients with systemic atherosclerosis. All of these issues could be overcome by tissue-engineered vascular grafts (TEVGs). A large body of evidence has recently emerged in support of TEVG technologies, introducing diverse cell sources (e.g., somatic cells and stem cells) and novel fabrication methods (e.g., scaffold-guided and self-assembled approaches). Before TEVG can be applied in a clinical setting, however, several aspects of the technology must be improved, such as the feasibility of obtaining cells, their biocompatibility and mechanical properties, and the time needed for fabrication, while the safety of supplemented materials, the patency and nonthrombogenicity of TEVGs, their growth potential, and the long-term influence of implanted TEVGs in the body must be assessed. Although recent advances in TEVG fabrication have yielded promising results, more research is needed to achieve the most feasible methods for generating optimal TEVGs. This article reviews multiple aspects of TEVG fabrication, including mechanical requirements, extracellular matrix components, cell sources, and tissue engineering approaches. The potential of periodic hydrostatic pressurization in the production of scaffold-free TEVGs with optimal elasticity and stiffness is also discussed. In the future, the integration of multiple technologies is expected to enable improved TEVG performance.

DOI： 10.34133/2021/1532103

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Other Link： http://downloads.spj.sciencemag.org/cbsystems/2021/1532103.xml
Scaffold-free tissue-engineered arterial grafts derived from human skeletal myoblasts. International journal

Junichi Saito, Utako Yokoyama, Takashi Nakamura, Tomomitsu Kanaya, Takayoshi Ueno, Yuji Naito, Toshio Takayama, Makoto Kaneko, Shigeru Miyagawa, Yoshiki Sawa, Yoshihiro Ishikawa

Artificial organs 45 ( 8 ) 919 - 932 2021.2

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Tissue-engineered vascular grafts (TEVGs) are in urgent demand for both adult and pediatric patients. Although several approaches have utilized vascular smooth muscle cells (SMCs) and endothelial cells as cell sources for TEVGs, these cell sources have a limited proliferative capacity that results in an inability to reconstitute neotissues. Skeletal myoblasts are attractive cell sources as they possess high proliferative capacity, and they are already being tested in clinical trials for patients with ischemic cardiomyopathy. Our previous study demonstrated that periodic hydrostatic pressurization (PHP) promoted fibronectin fibrillogenesis in vascular SMCs, and that PHP-induced extracellular matrix (ECM) arrangements enabled the fabrication of implantable arterial grafts derived from SMCs without using a scaffold material. We assessed the molecular response of human skeletal myoblasts to PHP exposure, and aimed to fabricate arterial grafts from the myoblasts by exposure to PHP. To examine the PHP-response genes, human skeletal myoblasts were subjected to bulk RNA-sequencing after PHP exposure. Gene-set enrichment analysis revealed significant positive correlations between PHP exposure and vascular development-related genes. Real-time polymerase chain reaction (RT-PCR) demonstrated that PHP significantly upregulated collagen and elastic fiber formation-related gene expression, such as fibronectin, lysyl oxidase, collagen type I α1, collagen type IV α1, and tropoelastin. Based on these findings showing the potential role of PHP in vessel formation, we fabricated arterial grafts by repeated cell seeding and exposure to PHP every 24 hours. The resultant 15-layered myoblast grafts had high collagen content, which provided a tensile rupture strength of 899 ± 104 mm Hg. Human skeletal myoblast grafts were implanted as patch grafts in the aorta of immunosuppressed rats and found to be endothelialized and completely patent until the endpoint of 60 postoperative days. Implanted human myoblasts were gradually replaced by host-derived cells, which successfully formed vascular neotissues with layered elastic fibers. These findings suggest that human skeletal myoblasts have the potential to be a feasible cell source for scaffold-free implantable arterial grafts under PHP culture conditions.

DOI： 10.1111/aor.13930

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Multilayered Human Skeletal Muscle Myoblast Sheets Promote the Healing Process After Colonic Anastomosis in Rats

Takashi Nakamura, Utako Yokoyama, Tomomitsu Kanaya, Takayoshi Ueno, Takanori Yoda, Atsushi Ishibe, Yuko Hidaka, Masanari Umemura, Toshio Takayama, Makoto Kaneko, Shigeru Miyagawa, Yoshiki Sawa, Itaru Endo, Yoshihiro Ishikawa

Cell Transplantation 30 096368972110095 - 096368972110095 2021.1

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Publishing type：Research paper (scientific journal) Publisher：SAGE Publications

Colorectal anastomotic leakage is one of the most feared and fatal complications of colorectal surgery. To date, no external coating material that can prevent anastomotic leakage has been developed. As myoblasts possess anti-inflammatory capacity and improve wound healing, we developed a multilayered human skeletal muscle myoblast (HSMM) sheet by periodic exposure to supraphysiological hydrostatic pressure during repeated cell seeding. We assessed whether the application of an HSMM sheet can promote the healing process after colonic anastomosis. Partial colectomy and insufficient suturing were employed to create a high-risk colo-colonic anastomosis model in 60 nude rats. Rats were divided into a control group ( n = 30) and an HSMM sheet group ( n = 30). Macroscopic findings, anastomotic bursting pressure, and histology at the colonic anastomotic site were evaluated on postoperative day (POD) 3, 5, 7, 14, and 28. The application of an HSMM sheet significantly suppressed abscess formation at the anastomotic site compared to the control group on POD3 and 5. The anastomotic bursting pressure in the HSMM sheet group was higher than that in the control group on POD3 and 5. Inflammatory cell infiltration in the HSMM sheet group was significantly suppressed compared to that in the control group throughout the time course. Collagen deposition in the HSMM sheet group on POD3 was significantly abundant compared to that in the control group. Regeneration of the mucosa at the colonic anastomotic site was promoted in the HSMM sheet group compared to that in the control group on POD14 and 28. Immunohistochemical analysis demonstrated that surviving cells in the HSMM sheet gradually decreased with postoperative time and none were detected on POD14. These results suggest that the application of a multilayered HSMM sheet may prevent postoperative colonic anastomotic leakage.

DOI： 10.1177/09636897211009559

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Other Link： http://journals.sagepub.com/doi/full-xml/10.1177/09636897211009559
Increased plasma levels of myosin heavy chain 11 is associated with atherosclerosis(和訳中)

高橋梨紗, 石上友章, 冨山博文, 近森大志郎, 菊池宏幸, 井上茂, 加藤優子, 田栗正隆, 石川義弘, 横山詩子

東京医科大学雑誌 79 ( 1 ) 104 - 104 2021.1

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ミオシン重鎖11の血漿中濃度上昇は動脈硬化と関連する(Increased plasma levels of myosin heavy chain 11 is associated with atherosclerosis)

高橋梨紗, 石上友章, 冨山博文, 近森大志郎, 菊池宏幸, 井上茂, 加藤優子, 田栗正隆, 石川義弘, 横山詩子

東京医科大学雑誌 79 ( 1 ) 104 - 104 2021.1

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2021&ichushi_jid=J00877&link_issn=&doc_id=20210924430042&doc_link_id=%2Fcr4tokyo%2F2021%2Fs07901%2F033%2F0104-0104%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fcr4tokyo%2F2021%2Fs07901%2F033%2F0104-0104%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif
低酸素周期的加圧培養によるヒト臍帯動脈平滑筋細胞を用いた人工血管の作製

小嶋朋之, 横山詩子, 中村隆, 齋藤純一, 石川義弘, 宮城悦子

東京医科大学雑誌 79 ( 1 ) 112 - 112 2021.1

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Language：Japanese Publisher：東京医科大学医学会

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Other Link： https://search-tp.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2021&ichushi_jid=J00877&link_issn=&doc_id=20210924430058&doc_link_id=%2Fcr4tokyo%2F2021%2Fs07901%2F049%2F0112-0112%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fcr4tokyo%2F2021%2Fs07901%2F049%2F0112-0112%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif
Doxorubicin directly induced fibrotic change of cardiac fibroblasts

Masanari Umemura, Masatoshi Narikawa, Ryo Tanaka, Hiroko Nemoto, Rina Nakakaji, Akane Nagasako, Yoshihiro Ishikawa

Folia Pharmacologica Japonica 156 ( 3 ) 146 - 151 2021

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Publishing type：Research paper (scientific journal) Publisher：Japanese Pharmacological Society

DOI： 10.1254/fpj.20101

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臍帯平滑筋細胞を用いた血管グラフトパッチの作製

小嶋朋之, 横山詩子, 依田崇典, 中村隆, 齋藤純一, 石川義弘, 宮城悦子

東京医科大学雑誌 78 ( 3 ) 301 - 301 2020.7

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Language：Japanese Publisher：東京医科大学医学会

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Other Link： https://search-tp.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2020&ichushi_jid=J00877&link_issn=&doc_id=20201113360054&doc_link_id=%2Fcr4tokyo%2F2020%2Fs07803%2F046%2F0301-0301%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fcr4tokyo%2F2020%2Fs07803%2F046%2F0301-0301%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif
Role of Tissue-Type Plasminogen Activator in Remodeling of the Ductus Arteriosus Invited Reviewed

Junichi Saito, Yoshihiro Ishikawa, Utako Yokoyama

Circulation Reports 2 ( 4 ) 211 - 217 2020.4

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Language：English Publishing type：Research paper (scientific journal) Publisher：Japanese Circulation Society

DOI： 10.1253/circrep.CR-20-0015

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Fabrication of implantable human arterial graft by periodic hydrostatic pressure Reviewed

Junichi Saito, Utako Yokoyama, Toshio Takayama, Hiroaki Ito, Tomomi Tadokoro, Yoshinobu Sugo, Kentaro Kurasawa, Miyuki Ogawa, Etsuko Miyagi, Hideki Taniguchi, Makoto Kaneko, Yoshihiro Ishikawa

Molecular Mechanism of Congenital Heart Disease and Pulmonary Hypertension 289 - 291 2020.2

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Prostaglandin E-EP4-mediated fibulin-1 up-regulation plays a role in intimal thickening of the ductus arteriosus

Satoko Ito, Utako Yokoyama, Junichi Saito, Munetaka Masuda, Toshihide Asou, Yoshihiro Ishikawa

Molecular Mechanism of Congenital Heart Disease and Pulmonary Hypertension 267 - 268 2020.1

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Language：English Publishing type：Part of collection (book) Publisher：Springer Singapore

DOI： 10.1007/978-981-15-1185-1_39

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Antenatal administration of betamethasone contributes to intimal thickening of the ductus arteriosus

Takahiro Kemmotsu, Utako Yokoyama, Junichi Saito, Satoko Ito, Azusa Uozumi, Shiho Iwasaki, Shigeru Nishimaki, Shuichi Ito, Munetaka Masuda, Toshihide Asou, Yoshihiro Ishikawa

Molecular Mechanism of Congenital Heart Disease and Pulmonary Hypertension 265 - 266 2020.1

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Language：English Publishing type：Part of collection (book) Publisher：Springer Singapore

DOI： 10.1007/978-981-15-1185-1_38

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アストロサイトに対するAMPK阻害と交流磁場併用効果についての腫瘍細胞との比較検討

秋本大輔, 梅村将就, 石川義弘, 山本哲哉

脳循環代謝 31 ( 1 ) 122 - 122 2019.11

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Language：Japanese Publisher：(一社)日本脳循環代謝学会

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プロスタグランディンE受容体EP4シグナルはLysyl oxydaseの発現を抑制し大動脈瘤の進行に関与する

廣見太郎, 横山詩子, 竹内一郎, 石川義弘

日本救急医学会雑誌 30 ( 9 ) 696 - 696 2019.9

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Minimally invasive thoracoscopic surgery for scimitar syndrome variant. Reviewed

Nitta M, Ishikawa Y, Machida D, Masuda M, Tamura K, Kimura K

Asian cardiovascular & thoracic annals 218492319865446 2019.7

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DOI： 10.1177/0218492319865446

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Translationally controlled tumor protein (TCTP) plays a pivotal role in cardiomyocyte survival through a Bnip3-dependent mechanism. Reviewed International journal

Cai W, Fujita T, Hidaka Y, Jin H, Suita K, Shigeta M, Kiyonari H, Umemura M, Yokoyama U, Sadoshima J, Ishikawa Y

Cell death & disease 10 ( 8 ) 549 - 549 2019.7

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Prevention of cardiomyocyte death is an important therapeutic strategy for heart failure. In this study, we focused on translationally controlled tumor protein (TCTP), a highly conserved protein that is expressed ubiquitously in mammalian tissues, including heart. TCTP plays pivotal roles in survival of certain cell types, but its function in cardiomyocytes has not been examined. We aimed to clarify the role of TCTP in cardiomyocyte survival and the underlying mechanism. Here, we demonstrated that downregulation of TCTP with siRNA induced cell death of cardiomyocytes with apoptotic and autophagic features, accompanied with mitochondrial permeability transition pore (mPTP) opening. TCTP loss did not induce cell death of cardiac fibroblasts. Bcl-2/adenovirus E1B 19-kDa interacting protein 3 (Bnip3) was found to mediate the TCTP-loss-induced cardiomyocyte death. In exploring the clinical significance of the TCTP expression in the heart, we found that DOX treatment markedly downregulated the protein expression of TCTP in cultured cardiomyocytes and in mouse heart tissue. Exogenous rescue of TCTP expression attenuated DOX-induced cardiomyocyte death. In mice, cardiomyocyte-specific overexpression of TCTP resulted in decreased susceptibility to DOX-induced cardiac dysfunction, accompanied with attenuated induction of Bnip3. Dihydroartemisinin, a pharmacological TCTP inhibitor, induced development of heart failure and cardiomyocyte death in control mice, but not in mice with cardiomyocyte-specific TCTP overexpression. Our findings revealed TCTP has a pivotal role in cardiomyocyte survival, at least in part through a Bnip3-dependent mechanism. TCTP could be considered as a candidate therapeutic target to prevent DOX-induced heart failure.

DOI： 10.1038/s41419-019-1787-7

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産学連携から生まれた市販医薬品磁性化技術を臨床応用するための研究

梅村将就, 勝亦真弓, 中鍛治里奈, 永迫茜, 石川義弘

臨床薬理の進歩 ( 40 ) 35 - 44 2019.6

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Language：Japanese Publisher：(公財)臨床薬理研究振興財団

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Correction to: Epac activation inhibits IL-6-induced cardiac myocyte dysfunction. Reviewed

Jin H, Fujita T, Jin M, Kurotani R, Hidaka Y, Cai W, Suita K, Prajapati R, Liang C, Ohnuki Y, Mototani Y, Umemura M, Yokoyama U, Sato M, Okumura S, Ishikawa Y

The journal of physiological sciences : JPS 69 ( 3 ) 557 - 557 2019.5

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The article Epac activation inhibits IL-6-induced cardiac myocyte dysfunction.

DOI： 10.1007/s12576-019-00661-0

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Epac1 deficiency inhibits basic fibroblast growth factor-mediated vascular smooth muscle cell migration. Reviewed

Yuko Kato, Utako Yokoyama, Takayuki Fujita, Masanari Umemura, Tetsuo Kubota, Yoshihiro Ishikawa

The journal of physiological sciences : JPS 69 ( 2 ) 175 - 184 2019.3

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Vascular smooth muscle cell (VSMC) migration and the subsequent intimal thickening play roles in vascular restenosis. We previously reported that an exchange protein activated by cAMP 1 (Epac1) promotes platelet-derived growth factor (PDGF)-induced VSMC migration and intimal thickening. Because basic fibroblast growth factor (bFGF) also plays a pivotal role in restenosis, we examined whether Epac1 was involved in bFGF-mediated VSMC migration. bFGF-induced lamellipodia formation and migration were significantly decreased in VSMCs obtained from Epac1-/- mice compared to those in Epac1+/+-VSMCs. The bFGF-induced phosphorylation of Akt and glycogen synthase kinase 3β (GSK3β), which play a role in bFGF-induced cell migration, was attenuated in Epac1-/--VSMCs. Intimal thickening induced by the insertion of a large wire was attenuated in Epac1-/- mice, and was accompanied by the decreased phosphorylation of GSK3β. These data suggest that Epac1 deficiency attenuates bFGF-induced VSMC migration, possibly via Akt/GSK3β pathways.

DOI： 10.1007/s12576-018-0631-7

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Antenatal Administration of Betamethasone Contributes to Intimal Thickening of the Rat Ductus Arteriosus. Reviewed

Takahiro Kemmotsu, Utako Yokoyama, Junichi Saito, Satoko Ito, Azusa Uozumi, Shigeru Nishimaki, Shiho Iwasaki, Kazuo Seki, Shuichi Ito, Yoshihiro Ishikawa

Circulation journal : official journal of the Japanese Circulation Society 83 ( 3 ) 654 - 661 2019.2

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BACKGROUND: Antenatal betamethasone (BMZ) is a standard therapy for reducing respiratory distress syndrome in preterm infants. Recently, some reports have indicated that BMZ promotes ductus arteriosus (DA) closure. DA closure requires morphological remodeling; that is, intimal thickening (IT) formation; however, the role of BMZ in IT formation has not yet been reported. Methods and Results: First, DNA microarray analysis using smooth muscle cells (SMCs) of rat preterm DA on gestational day 20 (pDASMCs) stimulated with BMZ was performed. Among 58,717 probe sets, ADP-ribosyltransferase 3 (Art3) was markedly increased by BMZ stimulation. Quantitative reverse transcription polymerase chain reaction (RT-PCR) confirmed the BMZ-induced increase of Art3 in pDASMCs, but not in aortic SMCs. Immunocytochemistry showed that BMZ stimulation increased lamellipodia formation. BMZ significantly increased total paxillin protein expression and the ratio of phosphorylated to total paxillin. A scratch assay demonstrated that BMZ stimulation promoted pDASMC migration, which was attenuated byArt3-targeted siRNAs transfection. pDASMC proliferation was not promoted by BMZ, which was analyzed by a 5'-bromo-2'-deoxyuridine (BrdU) assay. Whether BMZ increased IT formation in vivo was examined. BMZ or saline was administered intravenously to maternal rats on gestational days 18 and 19, and DA tissues were obtained on gestational day 20. The ratio of IT to tunica media was significantly higher in the BMZ-treated group. CONCLUSIONS: These data suggest that antenatal BMZ administration promotes DA IT through Art3-mediated DASMC migration.

DOI： 10.1253/circj.CJ-18-1033

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Hybrid metal complex nanocomposites for targeted cancer diagnosis and therapeutics

Jeong-Hwan Kim, Haruki Eguchi, Masanari Umemura, Yoshihiro Ishikawa

Materials for Biomedical Engineering: Inorganic Micro- and Nanostructures 427 - 461 2019.1

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Language：English Publishing type：Part of collection (book) Publisher：Elsevier

DOI： 10.1016/B978-0-08-102814-8.00015-9

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Usefulness of Exchanged Protein Directly Activated by cAMP (Epac)1-Inhibiting Therapy for Prevention of Atrial and Ventricular Arrhythmias in Mice. Reviewed

Prajapati R, Fujita T, Suita K, Nakamura T, Cai W, Hidaka Y, Umemura M, Yokoyama U, Knollmann BC, Okumura S, Ishikawa Y

Circulation journal : official journal of the Japanese Circulation Society 83 ( 2 ) 295 - 303 2019.1

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BACKGROUND: It has been suggested that protein directly activated by cAMP (Epac), one of the downstream signaling molecules of β-adrenergic receptor (β-AR), may be an effective target for the treatment of arrhythmia. However, there have been no reports on the anti-arrhythmic effects or cardiac side-effects of Epac1 inhibitors in vivo. Methods and Results: In this study, the roles of Epac1 in the development of atrial and ventricular arrhythmias are examined. In addition, we examined the usefulness of CE3F4, an Epac1-selective inhibitor, in the treatment of the arrhythmias in mice. In Epac1 knockout (Epac1-KO) mice, the duration of atrial fibrillation (AF) was shorter than in wild-type mice. In calsequestrin2 knockout mice, Epac1 deficiency resulted in a reduction of ventricular arrhythmia. In both atrial and ventricular myocytes, sarcoplasmic reticulum (SR) Ca2+ leak, a major trigger of arrhythmias, and spontaneous SR Ca2+ release (SCR) were attenuated in Epac1-KO mice. Consistently, CE3F4 treatment significantly prevented AF and ventricular arrhythmia in mice. In addition, the SR Ca2+ leak and SCR were significantly inhibited by CE3F4 treatment in both atrial and ventricular myocytes. Importantly, cardiac function was not significantly affected by a dosage of CE3F4 sufficient to exert anti-arrhythmic effects. CONCLUSIONS: These findings indicated that Epac1 is involved in the development of atrial and ventricular arrhythmias. CE3F4, an Epac1-selective inhibitor, prevented atrial and ventricular arrhythmias in mice.

DOI： 10.1253/circj.CJ-18-0743

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Reactive Fibrosis Precedes Doxorubicin-induced Heart Failure through Sterile Inflammation, and Pioglitazone Reduces Early Cardiac Remodelling Reviewed

Tanaka R, Umemura M, Narikawa M, Hikichi M, Osawa K, Fujita T, Yokoyama U, Ishigami T, Kimura K, Tamura K, Ishikawa Y

ESC Heart Failure. in press 2019

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Doxorubicin induces trans-differentiation and MMP1 expression in cardiac fibroblasts via cell death-independent pathways. Reviewed International journal

Narikawa M, Umemura M, Tanaka R, Hikichi M, Nagasako A, Fujita T, Yokoyama U, Ishigami T, Kimura K, Tamura K, Ishikawa Y

PloS one 14 ( 9 ) e0221940 2019

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Although doxorubicin (DOX)-induced cardiomyopathy causes lethal heart failure (HF), no early detection or effective treatment methods are available. The principal mechanisms of cardiotoxicity are considered to involve oxidative stress and apoptosis of cardiomyocytes. However, the effect of DOX on cardiac fibroblasts at non-lethal concentrations remains unknown. The aim of this study was to investigate the direct effect of doxorubicin on the activation of cardiac fibroblasts independent of cell death pathways. We first found that DOX induced α-SMA expression (marker of trans-differentiation) at a low concentration range, which did not inhibit cell viability. DOX also increased MMP1, IL-6, TGF-β and collagen expression in human cardiac fibroblasts (HCFs). In addition, DOX promoted Akt and Smad phosphorylation. A Smad inhibitor prevented DOX-induced α-SMA and IL-6 protein expression. An PI3K inhibitor also prevented MMP1 mRNA expression in HCFs. These findings suggest that DOX directly induces fibrotic changes in HCFs via cell death-independent pathways. Furthermore, we confirmed that these responses are organ- and species-specific for HCFs based on experiments using different types of human and murine fibroblast cell lines. These results suggest potentially new mechanisms of DOX-induced cardiotoxicity from the viewpoint of fibrotic changes in cardiac fibroblasts.

DOI： 10.1371/journal.pone.0221940

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A selective antagonist of prostaglandin E receptor subtype 4 attenuates abdominal aortic aneurysm. Reviewed

Mamun A, Yokoyama U, Saito J, Ito S, Hiromi T, Umemura M, Fujita T, Yasuda S, Minami T, Goda M, Uchida K, Suzuki S, Masuda M, Ishikawa Y

Physiological reports 6 ( 18 ) e13878 - e13878 2018.9

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Publishing type：Research paper (scientific journal) Publisher：Wiley

DOI： 10.14814/phy2.13878

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Alternating Magnetic Field (AMF) Enhances Cytotoxicity of Compound C. Reviewed International journal

Akimoto T, Umemura M, Nagasako A, Ohtake M, Fujita T, Yokoyama U, Eguchi H, Yamamoto T, Ishikawa Y

Cancer science 109 ( 11 ) 3483 - 3493 2018.8

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We previously reported the efficacy of anti-cancer therapy with hyperthermia using an alternating magnetic field (AMF) and a magnetic compound. In the course of the study, unexpectedly, we found that an AMF enhances the cytotoxicity of Compound C, an activated protein kinase (AMPK) inhibitor, although this compound is not magnetic. Therefore, we examined the cellular mechanism of AMF-induced cytotoxicity of Compound C in cultured human glioblastoma (GB) cells. An AMF (280 kHz, 250 Arms) for 30 minutes significantly enhanced the cytotoxicity of Compound C and promoted apoptosis towards several human GB cell lines in vitro. The AMF also increased Compound C-induced cell-cycle arrest of GB cells at the G2 phase and, thus, inhibited cell proliferation. The AMF increased Compound C-induced reactive oxygen species production. Furthermore, the AMF decreased ERK phosphorylation in the presence of Compound C and suppressed the protective autophagy induced by this compound. The application of an AMF in cancer chemotherapy may be a simple and promising method, which might reduce the doses of drugs used in future cancer treatment and, therefore, the associated side effects.

DOI： 10.1111/cas.13781

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Hydrostatic pressure suppresses fibrotic changes via Akt/GSK-3 signaling in human cardiac fibroblasts Reviewed

Ryo Tanaka, Masanari Umemura, Masatoshi Narikawa, Takayuki Fujita, Utako Yokoyama, Tomoaki Ishigami, Kazuo Kimura, Kouichi Tamura, Yoshihiro Ishikawa

Physiological Reports 6 ( 9 ) e13687 2018.5

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Language：English Publishing type：Research paper (scientific journal) Publisher：American Physiological Society

DOI： 10.14814/phy2.13687

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Epac activation inhibits IL-6-induced cardiac myocyte dysfunction Reviewed

Huiling Jin, Takayuki Fujita, Meihua Jin, Reiko Kurotani, Yuko Hidaka, Wenqian Cai, Kenji Suita, Rajesh Prajapati, Chen Liang, Yoshiki Ohnuki, Yasumasa Mototani, Masanari Umemura, Utako Yokoyama, Motohiko Sato, Satoshi Okumura, Yoshihiro Ishikawa

Journal of Physiological Sciences 68 ( 1 ) 77 - 87 2018.1

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Language：English Publishing type：Research paper (scientific journal) Publisher：Springer Tokyo

DOI： 10.1007/s12576-016-0509-5

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Tissue-type plasminogen activator contributes to remodeling of the rat ductus arteriosus Reviewed

Junichi Saito, Utako Yokoyama, Naoki Nicho, Yun-Wen Zheng, Yasuhiro Ichikawa, Satoko Ito, Masanari Umemura, Takayuki Fujita, Shuichi Ito, Hideki Taniguchi, Toshihide Asou, Munetaka Masuda, Yoshihiro Ishikawa

PLoS ONE 13 ( 1 ) e0190871 2018.1

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Language：English Publishing type：Research paper (scientific journal) Publisher：Public Library of Science

DOI： 10.1371/journal.pone.0190871

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Attenuation of ductus arteriosus intimal thickening in preterm sheep twins compared with singletons. Reviewed

Satoko Ito, Utako Yokoyama, Junichi Saito, Shinichi Sato, Haruo Usuda, Shimpei Watanabe, Ryuta Kitanishi, Yuichiro Miura, Masatoshi Saito, Takushi Hanita, Tadashi Matsuda, Yoshihiro Ishikawa

The journal of physiological sciences : JPS 67 ( 6 ) 723 - 729 2017.11

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Preterm twins have a higher morbidity rate of patent ductus arteriosus (PDA) than do singletons. However, the effect of multiple births on maturation of the ductus arteriosus (DA) has not been reported. Because intimal thickening (IT) is required for DA anatomical closure, we examined IT development in the DA of preterm twins and singletons. Sheep DA tissues obtained from preterm fetuses were subjected to elastica van Gieson staining to evaluate IT. The total IT score in each DA was the sum of the IT scores obtained from six evenly divided parts of the DA, which was positively correlated with gestational ages in singletons. Total IT scores were smaller in preterm twins than in singletons, although no difference in gestational age, birth weight, or gender ratio was observed. These data suggest that IT development of the DA is attenuated in sheep preterm twins, which may affect the higher morbidity of PDA.

DOI： 10.1007/s12576-017-0565-5

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薬効成分を磁性化した新規パクリタキセルを用いた口腔がん治療の開発

中鍛治里奈, 梅村将就, 大竹誠, 來生知, 江口晴樹, 藤内祝, 石川義弘

日本癌学会総会記事 76回 P - 1436 2017.9

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The iron chelating agent, deferoxamine detoxifies Fe(Salen)-induced cytotoxicity Reviewed

Masanari Umemura, Jeong-Hwan Kim, Haruki Aoyama, Yujiro Hoshino, Hidenobu Fukumura, Rina Nakakaji, Itaru Sato, Makoto Ohtake, Taisuke Akimoto, Masatoshi Narikawa, Ryo Tanaka, Takayuki Fujita, Utako Yokoyama, Masataka Taguri, Satoshi Okumura, Motohiko Sato, Haruki Eguchi, Yoshihiro Ishikawa

JOURNAL OF PHARMACOLOGICAL SCIENCES 134 ( 4 ) 203 - 210 2017.8

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DOI： 10.1016/j.jphs.2017.07.002

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Anticancer luminescent gold quantum clusters for in situ cancer-selective marking-imaging-targeting Reviewed

Jeong-Hwan Kim, Haruki Eguchi, Yoshihiro Ishikawa

NANOSCALE 9 ( 26 ) 9071 - 9082 2017.7

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DOI： 10.1039/c7nr02229h

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Transient receptor potential cation 3 channel regulates melanoma proliferation and migration Reviewed

Kayoko Oda, Masanari Umemura, Rina Nakakaji, Ryo Tanaka, Itaru Sato, Akane Nagasako, Chiaki Oyamada, Erdene Baljinnyam, Mayumi Katsumata, Lai-Hua Xie, Masatoshi Narikawa, Yukie Yamaguchi, Taisuke Akimoto, Makoto Ohtake, Takayuki Fujita, Utako Yokoyama, Kousaku Iwatsubo, Michiko Aihara, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 67 ( 4 ) 497 - 505 2017.7

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DOI： 10.1007/s12576-016-0480-1

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Cardiac overexpression of Epacl in transgenic mice rescues lipopolysaccharide-induced cardiac dysfunction and inhibits Jak-STAT pathway Reviewed

Huiling Jin, Takayuki Fujita, Meihua Jin, Reiko Kurotani, Iyuki Namekata, Shogo Hamaguchi, Yuko Hidaka, Wenqian Cai, Kenji Suita, Yoshiki Ohnuki, Yasumasa Mototani, Kouichi Shiozawa, Rajesh Prajapati, Chen Liang, Masanari Umemura, Utako Yokoyama, Motohiko Sato, Hikaru Tanaka, Satoshi Okumura, Yoshihiro Ishikawa

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY 108 170 - 180 2017.7

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DOI： 10.1016/j.yjmcc.2017.05.014

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Breast cancer information communicated on a public online platform: An analysis of ‘Yahoo! Answer Japan’ Reviewed

An Ohigashi, Salim Ahmed, Arfan R. Afzal, Naoko Shigeta, Helen Tam-Tham, Hideyuki Kanda, Yoshihiro Ishikawa, Tanvir C. Turin

Journal of Primary Health Care 9 ( 2 ) 167 - 172 2017.6

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Language：English Publishing type：Research paper (scientific journal) Publisher：CSIRO

DOI： 10.1071/HC16048

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Pathology and molecular mechanisms of coarctation of the aorta and its association with the ductus arteriosus Reviewed

Utako Yokoyama, Yasuhiro Ichikawa, Susumu Minamisawa, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 67 ( 2 ) 259 - 270 2017.3

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DOI： 10.1007/s12576-016-0512-x

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The role of Epac in the heart Reviewed

Takayuki Fujita, Masanari Umemura, Utako Yokoyama, Satoshi Okumura, Yoshihiro Ishikawa

CELLULAR AND MOLECULAR LIFE SCIENCES 74 ( 4 ) 591 - 606 2017.2

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DOI： 10.1007/s00018-016-2336-5

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Vidarabine, an Anti-Herpes Virus Agent, Protects Against the Development of Heart Failure With Relatively Mild Side-Effects on Cardiac Function in a Canine Model of Pacing-Induced Dilated Cardiomyopathy Reviewed

Takashi Nakamura, Takayuki Fujita, Megumi Kishimura, Kenji Suita, Yuko Hidaka, Wenqian Cai, Masanari Umemura, Utako Yokoyama, Masami Uechi, Yoshihiro Ishikawa

CIRCULATION JOURNAL 80 ( 12 ) 2496 - + 2016.12

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DOI： 10.1253/circj.CJ-16-0736

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Glutamate Promotes Contraction of the Rat Ductus Arteriosus Reviewed

Shujiro Fujita, Utako Yokoyama, Ryo Ishiwata, Rika Aoki, Kenji Nagao, Daiki Masukawa, Masanari Umemura, Takayuki Fujita, Shiho Iwasaki, Shigeru Nishimaki, Kazuo Seki, Shuichi Ito, Yoshio Goshima, Toshihide Asou, Munetaka Masuda, Yoshihiro Ishikawa

CIRCULATION JOURNAL 80 ( 11 ) 2388 - 2396 2016.11

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DOI： 10.1253/circj.CJ-16-0649

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Anticancer Nanomagnet-loaded Smart Nano-Ensembles for Magneto-Drug Delivery, MRI, and Hyperthermal Cancer Targeting Reviewed

J.-H. Kim, H. Eguchi, M. Umemura, Y. Ishikawa

Asia Nano 2016 at Sapporo Hokkaido Japan 2016.10

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薬効成分を磁性化した新規タキソールの口腔がん治療への応用

中鍛治里奈, 梅村将就, 佐藤格, 大竹誠, 小田香世子, 光藤健司, 來生知, 江口晴樹, 藤内祝, 石川義弘

日本癌学会総会記事 75回 P - 3274 2016.10

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Disruption of Epac1 protects the heart from adenylyl cyclase type 5-mediated cardiac dysfunction Reviewed

Wenqian Cai, Takayuki Fujita, Yuko Hidaka, Huiling Jin, Kenji Suita, Rajesh Prajapati, Chen Liang, Masanari Umemura, Utako Yokoyama, Motohiko Sato, Satoshi Okumura, Yoshihiro Ishikawa

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 475 ( 1 ) 1 - 7 2016.6

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DOI： 10.1016/j.bbrc.2016.04.123

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Role of phosphodiesterase 4 expression in the Epac1 signaling-dependent skeletal muscle hypertrophic action of clenbuterol Reviewed

Yoshiki Ohnuki, Daisuke Umeki, Yasumasa Mototani, Kouichi Shiozawa, Megumi Nariyama, Aiko Ito, Naoya Kawamura, Yuka Yagisawa, Huiling Jin, Wenqian Cai, Kenji Suita, Yasutake Saeki, Takayuki Fujita, Yoshihiro Ishikawa, Satoshi Okumura

Physiological Reports 4 ( 10 ) 2016.5

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DOI： 10.14814/phy2.12791

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The multiple roles of prostaglandin E2 in the regulation of the ductus arteriosus Reviewed

Utako Yokoyama, Susumu Minamisawa, Yoshihiro Ishikawa

Etiology and Morphogenesis of Congenital Heart Disease: From Gene Function and Cellular Interaction to Morphology 253 - 258 2016.1

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DOI： 10.1007/978-4-431-54628-3_35

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Norepinephrine-Induced Adrenergic Activation Strikingly Increased the Atrial Fibrillation Duration through beta 1-and alpha 1-Adrenergic Receptor-Mediated Signaling in Mice Reviewed

Kenji Suita, Takayuki Fujita, Nozomi Hasegawa, Wenqian Cai, Huiling Jin, Yuko Hidaka, Rajesh Prajapati, Masanari Umemura, Utako Yokoyama, Motohiko Sato, Satoshi Okumura, Yoshihiro Ishikawa

PLOS ONE 10 ( 7 ) e0133664 2015.7

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Establishment of successively transplantable rabbit VX2 cancer cells that express enhanced green fluorescent protein Reviewed

Hisashi Oshiro, Hidenobu Fukumura, Kiyotaka Nagahama, Itaru Sato, Kei Sugiura, Hiroaki Iobe, Emi Okiyama, Toshitaka Nagao, Yoji Nagashima, Ichiro Aoki, Shoji Yamanaka, Ayumi Murakami, Jiro Maegawa, Takashi Chishima, Yasushi Ichikawa, Yoshihiro Ishikawa, Takeshi Nagai, Masaharu Nomura, Kenichi Ohashi, Koji Okudela

MEDICAL MOLECULAR MORPHOLOGY 48 ( 1 ) 13 - 23 2015.3

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DOI： 10.1007/s00795-014-0071-2

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Eicosanoids and aortic aneurysm Reviewed

Utako Yokoyama, Ryo Ishiwata, Yoshihiro Ishikawa

Bioactive Lipid Mediators: Current Reviews and Protocols 267 - 278 2015.1

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DOI： 10.1007/978-4-431-55669-5_19

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Exendin-4 ameliorates cardiac ischemia/reperfusion injury via caveolae and caveolins-3 Reviewed

Yasuo M. Tsutsumi, Rie Tsutsumi, Eisuke Hamaguchi, Yoko Sakai, Asuka Kasai, Yoshihiro Ishikawa, Utako Yokoyama, Katsuya Tanaka

Cardiovascular Diabetology 13 ( 1 ) 132 2014.9

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DOI： 10.1186/s12933-014-0132-9

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Prostaglandin E2-EP4 plays a protective role against cardiac fibrosis Reviewed

R. Ishiwata, U. Yokoyama, S. Inoue, Y. Ichikawa, Y. Ishikawa

EUROPEAN HEART JOURNAL 35 1014 - 1014 2014.9

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Impaired nitric oxide production and increased blood pressure in systemic heterozygous ATP2B1 null mice Reviewed

Akira Fujiwara, Nobuhito Hirawa, Megumi Fujita, Yusuke Kobayashi, Yuki Okuyama, Keisuke Yatsu, Mari Katsumata, Yuichiro Yamamoto, Naoaki Ichihara, Sanae Saka, Yoshiyuki Toya, Gen Yasuda, Yoshio Goshima, Yasuharu Tabara, Tetsuro Miki, Hirotsugu Ueshima, Yoshihiro Ishikawa, Satoshi Umemura

JOURNAL OF HYPERTENSION 32 ( 7 ) 1415 - 1423 2014.7

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DOI： 10.1097/HJH.0000000000000206

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Expression of Concern Reviewed

Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 64 ( 3 ) 159 - 159 2014.5

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DOI： 10.1007/s12576-014-0308-9

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MRI造影剤フェルカルボトランを用いた新しい温熱化学療法の開発

佐藤格, 光藤健司, 梅村将就, 宮島章嘉, 中島英行, 來生知, 石川義弘, 藤内祝

頭頸部癌 40 ( 2 ) 271 - 271 2014.5

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Hyperthermia generated with ferucarbotran (Resovist(A (R))) in an alternating magnetic field enhances cisplatin-induced apoptosis of cultured human oral cancer cells Reviewed

Itaru Sato, Masanari Umemura, Kenji Mitsudo, Mitomu Kioi, Hideyuki Nakashima, Toshinori Iwai, Xianfeng Feng, Kayoko Oda, Akiyoshi Miyajima, Ayako Makino, Maki Iwai, Takayuki Fujita, Utako Yokoyama, Satoshi Okumura, Motohiko Sato, Haruki Eguchi, Iwai Tohnai, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 64 ( 3 ) 177 - 183 2014.5

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DOI： 10.1007/s12576-014-0309-8

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Geranylgeranylacetone protects the heart via caveolae and caveolin-3 Reviewed

Yasuo M. Tsutsumi, Rie Tsutsumi, Yousuke T. Horikawa, Yoko Sakai, Eisuke Hamaguchi, Yoshihiro Ishikawa, Utako Yokoyama, Asuka Kasai, Noriko Kambe, Katsuya Tanaka

LIFE SCIENCES 101 ( 1-2 ) 43 - 48 2014.4

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DOI： 10.1016/j.lfs.2014.02.019

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Three-dimensional multilayers of smooth muscle cells as a new experimental model for vascular elastic fiber formation studies Reviewed

Ryo Ishiwata, Utako Yokoyama, Michiya Matsusaki, Yoshiya Asano, Koji Kadowaki, Yasuhiro Ichikawa, Masanari Umemura, Takayuki Fujita, Susumu Minamisawa, Hiroshi Shimoda, Mitsuru Akashi, Yoshihiro Ishikawa

ATHEROSCLEROSIS 233 ( 2 ) 590 - 600 2014.4

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DOI： 10.1016/j.atherosclerosis.2014.01.045

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新規磁性体抗癌剤の抗腫瘍効果とそのメカニズム

佐藤格, 光藤健司, 梅村将就, 宮島章嘉, 中島英行, 來生知, 石川義弘, 藤内祝

Thermal Medicine 30 ( 1 ) 21 - 21 2014.3

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Protection of Cardiomyocytes from the Hypoxia-Mediated Injury by a Peptide Targeting the Activator of G-Protein Signaling 8 Reviewed

Motohiko Sato, Masahiro Hiraoka, Hiroko Suzuki, Miho Sakima, Abdullah Al Mamun, Yukiko Yamane, Takayuki Fujita, Utako Yokoyama, Satoshi Okumura, Yoshihiro Ishikawa

PLOS ONE 9 ( 3 ) e91980 2014.3

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DOI： 10.1371/journal.pone.0091980

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Store-Operated Ca2+ Entry (SOCE) Regulates Melanoma Proliferation and Cell Migration Reviewed

Masanari Umemura, Erdene Baljinnyam, Stefan Feske, Mariana S. De Lorenzo, Lai-Hua Xie, Xianfeng Feng, Kayoko Oda, Ayako Makino, Takayuki Fujita, Utako Yokoyama, Mizuka Iwatsubo, Suzie Chen, James S. Goydos, Yoshihiro Ishikawa, Kousaku Iwatsubo

PLOS ONE 9 ( 2 ) e89292 2014.2

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DOI： 10.1371/journal.pone.0089292

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A case of R-II-B type single coronary artery evaluated by multi-detector computed tomography and coronary angiography. Reviewed

Narikawa M, Kiyokuni M, Umemura M, Kawashima C, Doi H, Hisa A, Tomari S, Mitsuhashi T, Ishikawa Y, Endo T

Journal of Clinical and Experimental Cardiology 5 ( 10 ) 2014

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High-dose zoledronic acid narrows the periodontal space in rats Reviewed

Y. Okamoto, M. Hirota, Y. Monden, S. Murata, C. Koyama, K. Mitsudo, T. Iwai, Y. Ishikawa, I. Tohnai

International Journal of Oral and Maxillofacial Surgery 42 ( 5 ) 627 - 631 2013.5

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DOI： 10.1016/j.ijom.2012.11.011

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The roles of EP4 signaling in cardiac fibroblasts Reviewed

Shiori Inoue, Utako Yokoyama, Ryo Ishiwata, Jin Meihua, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S120 - S120 2013

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Controlled drug delivery and magnetic resonance imaging with intrinsic ferromagnetic nano-particle compound Reviewed

Eguchi, Haruki, Hirata, Kunio, Kurotani, Reiko, Fukumura, Hidenobu, Singh, David, Yamamoto, Masahiro, Sato, Itaru, Umemura, Masanori, Yamamoto, Masaki, Sato, Mamoru, Ishikawa, Yoshihiro

Journal of Pharmacological Sciences 121 125P 2013

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Anti-fibrotic Effect of Prostaglandin E2-EP4 in the Heart Reviewed

Ishiwata Ryo, Yokoyama Utako, Inoue Shiori, Ichikawa Yasuhiro, Ishikawa Yoshihiro

Circulation 128 ( Suppl 22 ) A16136 2013

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Proteomic analysis identified progtaglanid E 2-induced proteins in tissues from patients with aortic aneurysm Reviewed

Ryo Ishiwata, Utako Yokoyama, Noriaki Arakawa, Ayako Nomura, Toshio Ohsima, Susumu Minamisawa, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S119 - S119 2013

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Molecular Mechanisms of Dynamic Cardiovascular Adaptation from Fetal to Neonatal Life Reviewed

Utako Yokoyama, Jin Meihua, Rika Aoki, Ryo Ishiwata, Yasuhiro Ichikawa, Munetaka Masuda, Toshihide Aso, Susumu Minamisawa, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S81 - S81 2013

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Oxygenation-induced Postnatal Remodeling of the Ductus Arteriosus Reviewed

Jin MeiHua, Yokoyama Utako, Ishiwata Ryo, Minamisawa Susumu, Ishikawa Yoshihiro

CIRCULATION 126 ( 21 ) A8898 2012.11

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Pharmacological Stimulation of Type 5 Adenylyl Cyclase Stabilizes Heart Rate Under Both Microgravity and Hypergravity Induced by Parabolic Flight Reviewed

Yunzhe Bai, Takashi Tsunematsu, Qibin Jiao, Yoshiki Ohnuki, Yasumasa Mototani, Kouichi Shiozawa, Meihua Jin, Wenqian Cai, Hui-Ling Jin, Takayuki Fujita, Yasuhiro Ichikawa, Kenji Suita, Reiko Kurotani, Utako Yokoyama, Motohiko Sato, Kousaku Iwatsubo, Yoshihiro Ishikawa, Satoshi Okumura

JOURNAL OF PHARMACOLOGICAL SCIENCES 119 ( 4 ) 381 - 389 2012.8

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DOI： 10.1254/jphs.12102FP

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[How to overcome the crisis of American physiological society-advised from the former presidents]. Reviewed

Ishikawa Y, Marunaka Y

Nihon seirigaku zasshi. Journal of the Physiological Society of Japan 74 ( 4 ) 110 - 112 2012.7

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Prostaglandin E-2-EP4 Signaling Inhibits Vascular Elastic Fiber Formation in the Rodent Ductus Arteriosus. Reviewed

S. Minamisawa, U. Yokoyama, R. Ishiwata, Y. Sugimoto, H. Aoki, T. Nakamura, Y. Ishikawa

MOLECULAR BIOLOGY OF THE CELL 23 2012

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三次元血管モデルを用いた動脈硬化性疾患の機序解明 Reviewed

横山詩子, 石渡遼, 大島登志男, 南沢享, 石川義弘

科学と工業 86 ( 9 ) 329 - 335 2012

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Epac1 Deficiency Inhibit Neointima Formation After Vascular Injuryin vivo Reviewed

Kato Yuko, Yokoyama Utako, Okumura Satoshi, Minamisawa Susumu, Sata Masataka, Miyajima Eiji, Ishikawa Yoshihiro

CIRCULATION 124 ( 21 ) 2011.11

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ラットにおいて酸素誘導塩基性線維芽細胞増殖因子は動脈管の解剖学的閉鎖に寄与する(Oxygen-induced Basic Fibroblast Growth Factor Contributes to Anatomical Closure of the Rat Ductus Arteriosus)

Meihua Jin, Yokoyama Utako, Akaike Toru, Minamisawa Susumu, Ishikawa Yoshihiro

Circulation Journal 75 ( Suppl.I ) 153 - 153 2011.3

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The roles of cytochrome P450 in ischemic heart disease Reviewed

Motohiko Sato, Utako Yokoyama, Takayuki Fujita, Satoshi Okumura, Yoshihioro Ishikawa

Current Drug Metabolism 12 ( 6 ) 526 - 532 2011

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DOI： 10.2174/138920011795713715

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Prostaglandin EP4 Signaling Negatively Regulates Vascular Elastic Fiber Assembly in the Ductus Arteriosus Reviewed

Utako Yokoyama, Aki Shioda, Yuko Kato, Toshihide Asou, Hiroki Aoki, Tomoyuki Nakamura, Susumu Minamisawa, Yoshihiro Ishikawa

CIRCULATION 122 ( 21 ) 2010.11

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Accessory proteins for heterotrimeric G-protein: Implication in the cardiovascular system Reviewed

Motohiko Sato, Yoshihiro Ishikawa

Pathophysiology 17 ( 2 ) 89 - 99 2010.4

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DOI： 10.1016/j.pathophys.2009.03.011

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SERCA2aの発現および活性の低下による老化関連心機能障害においてsarcalumeninは重要な役割をもつ(Sarcalumenin Plays a Critical Role in Age-related Cardiac Dysfunction due to Decreases in SERCA2a Expression and Activity)

Jiao Qibin, Akaike Toru, Takeshima Hiroshi, Ishikawa Yoshihiro, Minamisawa Susumu

Circulation Journal 74 ( Suppl.I ) 160 - 160 2010.3

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T-type Ca2+ channels promote oxygenation-induced closure of the rat ductus arteriosus Reviewed

Toru Akaike, Utako Yokoyama, Yoshihiro Ishikawa, Susumu Minamisawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 60 S158 - S158 2010

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Disruption of Epac1 gene preserves cardiac function against pressure overload and chronic catecholamine stress Reviewed

Meihua Jin, Satoshi Okumura, Wenqian Cai, Yuko Hidaka, Reiko Kurotani, Utako Yokoyama, Motohiko Sato, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 60 S163 - S163 2010

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A case of giant coronary artery aneurysm and literature review Reviewed

Toshiaki Ebina, Yoshihiro Ishikawa, Keiji Uchida, Shinichi Suzuki, Kiyotaka Imoto, Jun Okuda, Kengo Tsukahara, Kiyoshi Hibi, Masami Kosuge, Shinichi Sumita, Yasuyuki Mochida, Toshiyuki Ishikawa, Kazuaki Uchino, Satoshi Umemura, Kazuo Kimura

JOURNAL OF CARDIOLOGY 53 ( 2 ) 293 - 300 2009.4

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DOI： 10.1016/j.jjcc.2008.07.015

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Effects of Targeted Disruption of the Type 5 Adenylyl Cyclase Gene Reviewed

Satoshi Okumura, Sayaka Suzuki, Yoshihiro Ishikawa

JOURNAL OF PHARMACOLOGICAL SCIENCES 109 ( 3 ) 354 - 359 2009.3

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DOI： 10.1254/jphs.08R26FM

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ラット動脈管においてアデニリルシクラーゼ6型はCAMP依存性血管リモデリングを選択的に促進するがアデニリルシクラーゼ2型及び5型にはその作用はない(Adenylyl Cyclase Type 6, but not Type 2 and 5, Selectively Promotes CAMP-dependent Vascular Remodeling in Rat Ductus Arteriosus)

Yokoyama Utako, Minamisawa Susumu, Katayama Ayako, Akaike Toru, Ishikawa Yoshihiro

Circulation Journal 73 ( Suppl.I ) 255 - 255 2009.3

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ラット動脈管開存における酸素化によるCa2+依存性平滑筋細胞移動の促進(Oxygenation Promotes Calcium-dependent Smooth Muscle Cell Migration in the Rat Ductus Arteriosus)

Akaike Toru, Yokoyama Utako, Iwamoto Mari, Ishikawa Yoshihiro, Minamisawa Susumu

Circulation Journal 73 ( Suppl.I ) 414 - 414 2009.3

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ADENYLYL CYCLASE TYPE 2 AND 6 DIFFERENTIALLY PROMOTE VASCULAR TONE AND REMODELING IN THE DUCTUS ARTERIOSUS Reviewed

Ayako Katayama, Utako Yokoyama, Toru Akaike, Susumu Minamisawa, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 59 458 - 458 2009

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A case of recurrent gastrointestinal stromal tumor of the stomach with complete response to imatinib mesilate Reviewed

Toru Aoyama, Hiroyuki Saeki, Jouji Samejima, Keita Fujii, Yoshihiro Ishikawa, Masakazu Kawamoto, Jun Fujisawa, Hiroshi Matsukawa, Yasushi Rino, Munetaka Masuda

Japanese Journal of Cancer and Chemotherapy 36 ( 6 ) 975 - 978 2009

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OXYGEN PROMOTES CALCIUM-DEPENDENT SMOOTH MUSCLE CELL MIGRATION IN THE RAT DUCTUS ARTERIOSUS Reviewed

Motoi Ozawa, Toru Akaike, Ayako Katayama, Utako Yokoyama, Yoshihiro Ishikawa, Susumu Minamisawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 59 323 - 323 2009

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Reversal effect of cyclic AMP on pro-fibrotic cardiac myofibroblasts Reviewed

Utako Yokoyama, Susumu Minamisawa, Yoshihiro Ishikawa

JOURNAL OF CARDIAC FAILURE 14 ( 7 ) S167 - S167 2008.9

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DOI： 10.1016/j.cardfail.2008.07.174

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ラット動脈管においてT型Ca2+チャンネル遮断による平滑筋細胞移動、内膜新生、及び酸素誘発性血管収縮の減弱化(Blockade of T-type calcium channels attenuates smooth muscle cell migration, neointimal formation, and oxygen-induced vascular contraction in rat ductus arteriosus)

Akaike Toru, Yokoyama Utako, Jin Mei Hua, Jiao Qibin, Iwamoto Mari, Ishikawa Yoshihiro, Minamisawa Susumu

日本小児循環器学会雑誌 24 ( 3 ) 491 - 491 2008.5

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EPAC promotes pathophysiological neointima formation in the rodent artery Reviewed

Susumu Minamisawa, Utako Yokoyama, Quan Hong, Toru Akaike, Masataka Sata, Yoshihiro Ishikawa

FASEB JOURNAL 22 2008.4

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Video-assisted thoracoscopic surgery for pulmonary arteriovenous malformations: Report of five cases Reviewed

Yoshihiro Ishikawa, Kazuki Yamanaka, Teppei Nishii, Keita Fujii, Yasushi Rino, Takamitsu Maehara

General Thoracic and Cardiovascular Surgery 56 ( 4 ) 187 - 190 2008.4

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DOI： 10.1007/s11748-007-0215-6

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筋小胞体内カルシウム結合蛋白質sarcalumenin欠損マウスの心機能に与える加齢などの生理学的ストレスの影響(The effect of physiological stresses such as aging on cardiac function in sarcalumenin-deficient mice)

Jiao Qibin, Shimura Miei, Akaike Toru, Takeshima Hiroshi, Ishikawa Yoshihiro, Minamisawa Susumu

The Journal of Physiological Sciences 58 ( Suppl. ) S185 - S185 2008.4

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ラット動脈管における平滑筋細胞移動の成長ホルモンによる増加(Growth hormone increases migration of smooth muscle cells in rat ductus arteriosus)

Jin Meihua, Akaike Toru, Quan Hong, Jiao Qibin, Iwasaki Shiho, Ishikawa Yoshihiro, Minamisawa Susumu

The Journal of Physiological Sciences 58 ( Suppl. ) S189 - S189 2008.4

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ラット動脈管における平滑筋細胞移動における酸素圧上昇の役割(A role of rising oxygen tension on smooth muscle cell migration in the rat ductus arteriosus)

Akaike Toru, Yokoyama Utako, Jiao Qibin, Jin Mei Hua, Quan Hong, Ishikawa Yoshihiro, Minamisawa Susumu

The Journal of Physiological Sciences 58 ( Suppl. ) S189 - S189 2008.4

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ラット動脈管における酸素分圧上昇による平滑筋細胞遊走の促進(Rising Oxygen Tension Promoted Smooth Muscle Cell Migration in the Rat Ductus Arteriosus)

Akaike Toru, Yokoyama Utako, Iwamoto Mari, Satoh Motohiko, Ishikawa Yoshihiro, Minamisawa Susumu

Circulation Journal 72 ( Suppl.I ) 621 - 621 2008.3

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Interleukin-15 inhibits smooth muscle cell proliferation and hyaluronan production in rat ductus arteriosus Reviewed

Shiho Iwasaki, Susumu Minamisawa, Utako Yokoyama, Toru Akaike, Hong Quan, Yoji Nagashima, Shigeru Nishimaki, Yoshihiro Ishikawa, Shumpei Yokota

PEDIATRIC RESEARCH 62 ( 4 ) 392 - 398 2007.10

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DOI： 10.1203/PDR.0b013e31813c9339

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Maternal vitamin A alters gene profiles and structural maturation of the rat ductus arteriosus Reviewed

Utako Yokoyama, Yoji Sato, Toru Akaike, Seiichi Ishida, Junichi Sawada, Taku Nagao, Hong Quan, Meihua Jin, Mari Iwamoto, Shumpei Yokota, Yoshihiro Ishikawa, Susumu Minamisawa

PHYSIOLOGICAL GENOMICS 31 ( 1 ) 139 - 157 2007.9

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DOI： 10.1152/physiolgenomics.00007.2006

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cAMP-mediated regulation of CYP enzymes and its application in chemotherapy. Reviewed

Ishikawa Y, Suzuki S, Otsu K, Ulucan C, Iwatsubo K, Eguchi H

Drug metabolism letters 1 176 - 178 2007.8

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ラットDAの酸素誘導性血管収縮と平滑筋細胞の遊走のT型カルシウムチャンネルによる制御(T-type calcium channels regulate oxygen-induced vascular contraction and smooth muscle cell migration in the rat DA)

Akaike Toru, Yokoyama Utako, Quan Hong, Ishikawa Yoshihiro, Minamisawa Susumu

The Journal of Physiological Sciences 57 ( Suppl. ) S80 - S80 2007.4

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Epac1は平滑筋細胞遊走を促進することによりラット動脈管の内膜クッション形成を促進する(Epac1 Promotes Intimal Cushion Formation of the Rat Ductus Arteriosus by Enhancing Smooth Muscle Cell Migration)

Akaike Toru, Yokoyama Utako, Quan Hong, Iwamoto Mari, Ishikawa Yoshihiro, Minamisawa Susumu

Circulation Journal 71 ( Suppl.I ) 190 - 190 2007.3

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ラット動脈管における酸素による血管収縮及び平滑筋細胞遊走のTタイプカルシウムチャネルによる制御(T-type Calcium Channels Regulate Oxygen-induced Vascular Contraction and Smooth Muscle Cell Migration in the Rat Ductus Arteriosus)

Akaike Toru, Yokoyama Utako, Quan Hong, Iwamoto Mari, Ishikawa Yoshihiro, Minamisawa Susumu

Circulation Journal 71 ( Suppl.I ) 139 - 139 2007.3

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Caveolin-3 inhibits growth signal in cardiac myoblasts in a Ca2+-dependent manner Reviewed

Takayuki Fujita, Kouji Otsu, An Oshikawa, Hideaki Hori, Hitoshi Kitamura, Takaaki Ito, Satoshi Umemura, Susumu Minamisawa, Yoshihiro Ishikawa

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 10 ( 1 ) 216 - 224 2006.1

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DOI： 10.1111/j.1582-4934.2006.tb00302.x

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An unusual transesophageal echocardiographic finding after surgical correction of a coronary artery fistula Reviewed

Y Ishikawa, Y Niimi, S Morita

JOURNAL OF CARDIOTHORACIC AND VASCULAR ANESTHESIA 19 ( 5 ) 693 - 694 2005.10

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DOI： 10.1053/j.jvca.2005.06.009

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Mechanical stress-dependent transcriptional regulation of sarcolipin gene in the rodent atrium Reviewed

M Shimura, S Minamisawa, U Yokoyama, S Umemura, Y Ishikawa

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 334 ( 3 ) 861 - 866 2005.9

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DOI： 10.1016/j.bbrc.2005.06.186

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Disruption of type 5 adenylyl cyclase negates the developmental increase in G alpha olf expression in the striatum Reviewed

T Iwamoto, K Iwatsubo, S Okumura, Y Hashimoto, T Tsunematsu, Y Toya, D Herve, S Umemura, Y Ishikawa

FEBS LETTERS 564 ( 1-2 ) 153 - 156 2004.4

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DOI： 10.1016/S0014-5793(04)00333-3

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[High blood pressure and cardiac hypertrophy] Reviewed

Ishikawa Y

Nippon rinsho. Japanese journal of clinical medicine 62 Suppl 3 342 - 346 2004.3

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Polymorphism of the type 6 adenylyl cyclase gene and cardiac hypertrophy Reviewed

E Ikoma, T Tsunematsu, Nakazawa, I, T Shiwa, K Hibi, T Ebina, Y Mochida, Y Toya, H Hori, K Uchino, S Minamisawa, K Kimura, S Umemura, T Ishikawa

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY 42 S27 - S32 2003.12

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Ischemic preconditioning prevents ischemia-induced beta-adrenergic receptor sequestration Reviewed

K Iwatsubo, Y Toya, T Fujita, T Ebina, C Schwencke, S Minamisawa, S Umemura, Y Ishikawa

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY 35 ( 8 ) 923 - 929 2003.8

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DOI： 10.1016/S0022-2828(03)00173-1

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Isoform-specific regulation of adenylyl cyclase: a potential target in future pharmacotherapy Reviewed

K Iwatsubo, T Tsunematsu, Y Ishikawa

EXPERT OPINION ON THERAPEUTIC TARGETS 7 ( 3 ) 441 - 451 2003.6

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DOI： 10.1517/14728222.7.3.441

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Characterization of beta-adrenergic receptor sequestration by newly developed whole cell binding assays Reviewed

K Iwatsubo, Y Tao, T Onda, T Toya, T Schwencke, T Fujita, T Ebina, T Iwamoto, H Hori, S Minamisawa, S Umemura, Y Ishikawa

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY 41 S53 - S56 2003.1

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Isoform-targeted regulation of cardiac adenylyl cyclase Reviewed

Y Ishikawa

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY 41 S1 - S4 2003.1

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Diabetes is not a potent inducer of neuronal cell death in mouse sensory ganglia, but it enhances neurite regeneration in vitro Reviewed

K Sango, H Horie, H Saito, K Ajiki, A Tokashiki, K Takeshita, Y Ishigatsubo, H Kawano, Y Ishikawa

LIFE SCIENCES 71 ( 20 ) 2351 - 2368 2002.10

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DOI： 10.1016/S0024-3205(02)02040-4

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Clinical implications of cardiac (123)I-meta-iodobenzylguanidine scintigraphy and cardiac natriuretic peptides in patients with heart disease. International journal

Toshiaki Ebina, N Takahashi, I Mitani, S Sumita, T Ishigami, K Ashino, K Minamisawa, N Kuji, H Ochiai, Y Ishikawa, T Oka, T Inoue, S Matsubara, S Umemura

Nuclear medicine communications 23 ( 8 ) 795 - 801 2002.8

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The purpose of this study was to evaluate whether or not cardiac sympathetic nerve activity, using (123)I-meta-iodobenzylguanidine ((123)I-MIBG) imaging, and cardiac natriuretic peptides (atrial and brain, ANP and BNP) were independent predictors of cardiac events, and, if so, which was the stronger predictor. Planar (123)I-MIBG images were obtained from 62 patients with heart disease. Plasma ANP and BNP levels, left ventricular ejection fraction (LVEF) by echocardiography, serum total cholesterol and triglyceride were measured. (123)I-MIBG was assessed as the heart-to-mediastinum (H/M) ratio of the delayed image and the washout rate (WoR) from the early to the delayed image. Patients were followed up for an average of 16.2 months, and 12 of 62 patients had cardiac events. Patients with events had significantly lower LVEF and H/M ratio compared with those without events. They had significantly higher WoR, ANP and BNP. By multivariate Cox proportional hazard analysis, (123)I-MIBG (H/M or WoR), ANP and BNP were independent predictors for cardiac events. Event-free survival using a Kaplan-Meier model, with a threshold value of 2.0 for H/M and 45% for WoR, showed that patients with H/M<2.0 and/or WoR>45% had a significantly poorer prognosis. These results suggest that (123)I-MIBG imaging and cardiac natriuretic peptides are useful tools for the evaluation of patients with heart disease, and that cardiac sympathetic nerve activity is a stronger predictor of cardiac events.

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Trachea enhances neurite regeneration from adult rat nodose ganglia in vitro

H Saito, K Sango, H Horie, K Takeshita, H Ikeda, Y Ishigatsubo, Y Ishikawa

LIFE SCIENCES 70 ( 16 ) 1935 - 1946 2002.3

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DOI： 10.1016/S0024-3205(02)01498-4

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Changes in caveolin subtype protein expression in aging rat organs Reviewed

J Kawabe, BS Grant, M Yamamoto, C Schwencke, S Okumura, Y Ishikawa

MOLECULAR AND CELLULAR ENDOCRINOLOGY 176 ( 1-2 ) 91 - 95 2001.5

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IL-6 up-regulates CNTF mRNA expression and enhances neurite regeneration

T Shuto, H Horie, N Hikawa, K Sango, A Tokashiki, H Murata, Yamamoto, I, Y Ishikawa

NEUROREPORT 12 ( 5 ) 1081 - 1085 2001.4

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DOI： 10.1097/00001756-200104170-00043

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Interleukin-12 promotes neurite outgrowth in mouse sympathetic superior cervical ganglion neurons Reviewed

HY Lin, N Hikawa, T Takenaka, Y Ishikawa

NEUROSCIENCE LETTERS 278 ( 3 ) 129 - 132 2000.1

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Diabetes alters neurite regeneration from mouse retinal explants in culture

Masahiko Takano, Kazunori Sango, Kazunori Sango, Hidenori Horie, Mayumi Sato, Yasuhito Iijima, Shigeaki Ohno, Shuji Inoue, Yoshihiro Ishikawa

Neuroscience Letters 275 175 - 178 1999.11

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Enhanced neural regeneration from transected vagus nerve terminals in diabetic mice in vitro

H Saito, K Sango, H Horie, H Ikeda, Y Ishigatsubo, Y Ishikawa, S Inoue

NEUROREPORT 10 ( 5 ) 1025 - 1028 1999.4

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DOI： 10.1097/00001756-199904060-00024

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Caveolin is an inhibitor of platelet-derived growth factor receptor signaling Reviewed

M Yamamoto, Y Toya, RA Jensen, Y Ishikawa

EXPERIMENTAL CELL RESEARCH 247 ( 2 ) 380 - 388 1999.3

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Downregulation of caveolin expression by cAMP signal Reviewed

M Yamamoto, S Okumura, N Oka, C Schwencke, Y Ishikawa

LIFE SCIENCES 64 ( 15 ) 1349 - 1357 1999.3

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Caveolin is an activator of insulin receptor signaling Reviewed

M Yamamoto, Y Toya, C Schwencke, MP Lisanti, MG Myers, Y Ishikawa

JOURNAL OF BIOLOGICAL CHEMISTRY 273 ( 41 ) 26962 - 26968 1998.10

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Forskolin derivatives with increased selectivity for cardiac adenylyl cyclase Reviewed

Y Toya, C Schwencke, Y Ishikawa

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY 30 ( 1 ) 97 - 108 1998.1

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Regulation of adenylyl cyclase isoforms by N-alkanols Reviewed

T Ebina, Y Toya, J Kawabe, Y Ishikawa

JOURNAL OF CELLULAR BIOCHEMISTRY 66 ( 4 ) 450 - 456 1997.9

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beta-adrenergic receptor signalling in stunned myocardium of conscious pigs Reviewed

S Sato, N Sato, RK Kudej, M Uechi, K Asai, YT Shen, Y Ishikawa, SF Vatner, DE Vatner

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY 29 ( 5 ) 1387 - 1400 1997.5

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DOI： 10.1006/jmcc.1997.0377

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Isoform specific regulation of adenylyl cyclase by oxidized catecholamines Reviewed

T Ebina, Y Toya, N Oka, C Schwencke, J Kawabe, Y Ishikawa

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY 29 ( 4 ) 1247 - 1254 1997.4

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Conformation-dependent activation of type II adenylyl cyclase by protein kinase C Reviewed

T Ebina, J Kawabe, T Katada, S Ohno, CJ Homcy, Y Ishikawa

JOURNAL OF CELLULAR BIOCHEMISTRY 64 ( 3 ) 492 - 498 1997.3

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Regulation of type V adenylyl cyclase by PMA-sensitive and -insensitive protein kinase C isoenzymes in intact cells Reviewed

J Kawabe, T Ebina, Y Toya, N Oka, C Schwencke, E Duzic, Y Ishikawa

FEBS LETTERS 384 ( 3 ) 273 - 276 1996.4

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Current Topics in Heterotrimeric GTP-binding Proteins. Multiplicity of adenylylcyclase and regulation of G-protein.

ISHIKAWA Yoshihiro

Folia Pharmacologica Japonica 103 ( 6 ) 285 - 293 1994

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Language：Japanese Publisher：The Japanese Pharmacological Society

Adenylylcyclase is a membrane bound enzyme that catalyzes the conversion of ATP to cyclic AMP. Studies on the regulation of adenylylcyclase have been hampered by the small amount of this enzyme in the cell as well as by the instability of the catalytic activity. Cloning of multiple adenylylcyclase isoforms (types I though VIII) has indicated the presence of a large enzyme family, which is further subdivided into several smaller groups. Members within the same group share similar biochemical properties. The multiplicity of adenylylcyclase is made through at least three distinct mechanisms. First, each isoform is encoded by a distinct gene. Second, multiple isoforms are generated through possible alternative splicing from the same gene. Third, there is a mechanism to generate a half-molecule of adenylylcyclase via alternative polyadenylation. Overexpression of a distinct isoform in insect cells followed by purification has enabled researchers to examine the role of each specific isoform in vitro. The results have suggested that each isoform is regulated through distinct mechanisms. For example, type I adenylylcyclase is inhibited in the presence of βγ-subunits, while type II is stimulated. Other isoforms such as types V and VI are not affected. On the other hand, Giα may directly inhibit each adenylylcyclase isoform. Further characterization of adenylylcyclase would be feasible using those clones in the future.

DOI： 10.1254/fpj.103.285

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CHARACTERISTIC LOCALIZATION OF ALPHA(1)-ADRENOCEPTORS AND ALPHA(2)-ADRENOCEPTORS IN THE HUMAN KIDNEY Reviewed

K MINAMISAWA, S UMEMURA, N HIRAWA, S HAYASHI, Y TOYA, Y ISHIKAWA, G YASUDA, M ISHII

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY 20 ( 7-8 ) 523 - 526 1993.7

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Adenylylcyclase: Characterization in the Heart and Its Regulation in Heart Failure.

Homcy Charles J., Katsushika Shuichi, Kawabe Jun-ichi, Kiuchi Kaname, Komamura Kazuo, Vatner Dorothy E., Vatner Stephen F., Ishikawa Yoshihiro

Hypertension Research 16 ( 2 ) 79 - 83 1993

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Language：English Publisher：The Japanese Society of Hypertension

It is generally acknowledged that heart failure is characterized by several disorders in cardiac autonomic properties, including sympathetic, parasympathetic and baroreceptor responses. Part of the mechanism of altered cardiovascular control and reduced catecholamine responsiveness in heart failure involves changes in end-organ responses mediated via beta adrenergic receptors. We have now determined the changes that occur in these components during the inception of heart failure induced by cardiac pacing. First, we quantitiated the stoichiometry and function of each of the components of the beta-adrenergic signaling pathway, including the receptor itself, Gs and the adenylylcyclase catalyst. Two key abnormalities occur: (1) the receptor uncouples from Gs, as indicated by loss of high affinity agonist binding sites without a change in receptor density; (2) there is an associated loss adenylylcyclase catalytic activity without any change in the concentration or function of the stimulatory GTP-binding protein Gs. To understand, therefore, what factors underlie the loss in adenylylcyclase catalytic activity; i.e., whether these are the results of a reduced concentration of the catalyst or due to its post-translational modification, we first cloned the cardiac isoforms of adenylylcyclase. Two novel adenylylcyclase cDNAs, types V and VI, were identified that share the motif of tandem six-transmembrane spans separated by a large hydrophilic cytoplasmic loop. Our data suggest that a decrease in the content of the adenylylcyclase catalyst itself contributes to impaired cyclic AMP production in heart failure and may represent a fundamental defect contributing to a progressive decline in LV function. (Hypertens Res 1993; 16: 79-83)

DOI： 10.1291/hypres.16.79

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IDENTIFICATION OF AN ALPHA2-ADRENOCEPTOR IN HUMAN CORONARY-ARTERIES BY RADIOLIGAND BINDING ASSAY Reviewed

Y ISHIKAWA, S UMEMURA, K UCHINO, T SHINDOU, G YASUDA, K MINAMISAWA, S HAYASHI, N HIRAWA, M ISHII

LIFE SCIENCES 48 ( 26 ) 2513 - 2518 1991

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Measurement of plasma active renin by solid phase radioimmunoassay using monoclonal antibodies Reviewed

H. Shionoiri, I. Takasaki, Y. Ishikawa, K. Minamisawa, K. I. Sugimoto, N. Hirawa, S. I. Ueda, E. Gotoh

American Journal of the Medical Sciences 300 ( 3 ) 138 - 143 1990

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DOI： 10.1097/00000441-199009000-00002

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ALPHA-2-ADRENOCEPTOR STIMULATION INHIBITS CELLULAR CYCLIC-AMP PRODUCTION IN MICRODISSECTED HUMAN GLOMERULI Reviewed

S UMEMURA, N HIRAWA, Y TOYA, K MINAMIZAWA, G YASUDA, Y ISHIKAWA, S HAYASHI, M ISHII

CLINICAL AND EXPERIMENTAL HYPERTENSION PART A-THEORY AND PRACTICE 11 275 - 280 1989

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Alpha 2-adrenoceptor stimulation inhibits cellular cyclic AMP production in microdissected human glomeruli Reviewed

S. Umemura, N. Hirawa, Y. Toya, K. Minamizawa, G. Yasuda, Y. Ishikawa, S. Hayashi, M. Ishii

Clinical and Experimental Hypertension A11 ( 1 ) 275 - 280 1989

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DOI： 10.3109/10641968909045431

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Functional atrial natriuretic peptide receptor in human adrenal tumor Reviewed

H. Shionoiri, N. Hirawa, I. Takasaki, Y. Ishikawa, H. Oda, K. Minamisawa, K. Sugimoto, T. Matsukawa, S. Ueda, E. Miyajima, S. Umemura, E. Gotoh, M. Ishii, M. Ishido, M. Shimonaka, S. Hirose

Journal of Cardiovascular Pharmacology 13 ( 6 ) S9 - S12 1989

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DOI： 10.1097/00005344-198905006-00004

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INHIBITORY EFFECT OF HUMAN ATRIAL NATRIURETIC PEPTIDE ON CYCLIC-AMP LEVELS IN MICRODISSECTED HUMAN GLOMERULI Reviewed

S UMEMURA, Y TOYA, N HIRAWA, Y ISHIKAWA, K MINAMIZAWA, G YASUDA, S HAYASHI, M ISHII

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY 13 S36 - S38 1989

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Lack of atrial natriuretic peptide receptors in human aldosteronoma Reviewed

H. Shionoiri, N. Hirawa, I. Takasaki, Y. Ishikawa, H. Oda, E. Gotoh, M. Hosaka, M. Shimonaka, M. Ishido, S. Hirose

Biochemical and Biophysical Research Communications 152 ( 1 ) 37 - 43 1988.4

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DOI： 10.1016/S0006-291X(88)80676-4

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Presence of functional receptors for atrial natriuretic peptide in human pheochromocytoma Reviewed

H. Shionoiri, N. Hirawa, I. Takasaki, Y. Ishikawa, K. Minamisawa, E. Miyajima, Y. Kinoshita, K. Shimoyama, M. Shimonaka, M. Ishido, S. Hirose

Biochemical and Biophysical Research Communications 148 ( 1 ) 286 - 291 1987.10

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DOI： 10.1016/0006-291X(87)91108-9

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IDENTIFICATION OF AN ATRIAL-NATRIURETIC-PEPTIDE SPECIFIC RECEPTOR IN HUMAN-KIDNEY Reviewed

Y ISHIKAWA, S UMEMURA, G YASUDA, K UCHINO, T SHINDOU, K MINAMIZAWA, Y TOYA, Y KANEKO

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 147 ( 1 ) 135 - 139 1987.8

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EXISTENCE OF RENAL ALPHA-1-ADRENOCEPTORS AND ALPHA-2-ADRENOCEPTORS IN THE HUMAN-KIDNEY - RADIOLIGAND BINDING STUDY IN MEMBRANES FROM THE HUMAN RENAL-CORTEX AND MEDULLA Reviewed

S UMEMURA, G YASUDA, K UCHINO, T SHINDO, Y ISHIKAWA, Y TOYA, Y KANEKO

JOURNAL OF HYPERTENSION 4 S222 - S225 1986.12

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ガイトン生理学

Hall, John E. (John Edward), 石川, 義弘, 岡村, 康司, 尾仲, 達史, 河野, 憲二, 金子, 猛(呼吸器内科学), 北村, 義浩, 藤乗, 嗣泰, 松嶋, 成志

エルゼビア・ジャパン 2018.3 （ ISBN:9784860347741 ）

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Total pages：xix, 1059p Language：Japanese

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市場原理とアメリカ医療―日本の医療改革の未来形自由競争・医療格差社会を生き抜くアメリカ式医療経営入門

石川義弘（ Role： Sole author）

医学通信社 2007.7 （ ISBN:4870583658 ）

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Total pages：290

ASIN

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低酸素下周期加圧によるヒト血管平滑筋細胞由来人工血管の作製

小嶋朋之, 中村隆, 齋藤純一, 日高祐子, 井上華, 横山詩子, 秋本大輔, CHICK Christian Nanga, 臼杵豊展, 金子真, 小嶋朋之, 宮城悦子, 石川義弘

東京医科大学雑誌(Web) 82 ( 2 ) 2024

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低酸素下加圧培養によるヒト臍帯動脈平滑筋細胞由来の人工血管の作製

小嶋朋之, 小嶋朋之, 齋藤純一, 中村隆, 井上華, 石川義弘, 横山詩子

日本小児循環器学会総会・学術集会(Web) 58th 2022

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プロスタグランディンE受容体EP4シグナルはLysyl oxydaseの発現を抑制し大動脈瘤の進行に関与する

廣見太郎, 横山詩子, 竹内一郎, 石川義弘

日本救急医学会雑誌 30 ( 9 ) 696 - 696 2019.9

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内皮細胞が誘導する一方向性平滑筋細胞遊走が動脈管内膜肥厚を形成する

伊藤智子, 横山詩子, 横山詩子, 中川路太一, 齋藤純一, 二町尚樹, 益田宗孝, 麻生俊英, 石川義弘

日本小児循環器学会雑誌 35 ( Supplement 1 ) s1.167 - 167 2019.6

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動脈管平滑筋細胞間由来Fibulin‐1は内皮由来Versicanと共役して動脈管内膜肥厚形成を促進する

伊藤智子, 横山詩子, 横山詩子, 石川義弘

日本結合組織学会学術大会抄録集 51st 133 - 133 2019.5

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急性と慢性:心不全はどこがちがうのか?

石川義弘, 藤田孝之, 梅村将就, 横山詩子

Shock 33 ( 2 ) 34 - 39 2019.2

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【心血管のトランスレーショナルリサーチ】周期加圧培養法による人工血管の作成

石川義弘, 齋藤純一, 横山詩子, 金子真

循環制御 39 ( 3 ) 155 - 156 2019.1

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アストロサイトに対するAMPK阻害と交流磁場併用効果についての腫瘍細胞との比較検討

秋本大輔, 秋本大輔, 秋本大輔, 梅村将就, 石川義弘, 山本哲哉

脳循環代謝(Web) 31 ( 1 ) 2019

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ラット母体への分娩前ベタメタゾン投与が動脈管内膜肥厚へ与える作用の検討

釼持孝博, 釼持孝博, 横山詩子, 齋藤純一, 伊藤智子, 魚住梓, 岩崎志穂, 西巻滋, 関和男, 石川義弘

日本新生児成育医学会雑誌 30 ( 3 ) 608 - 608 2018.10

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動脈管閉鎖における内皮機能の役割

齋藤純一, 横山詩子, 益田宗孝, 麻生俊英, 石川義弘

日本小児循環器学会雑誌 34 ( Supplement 1 ) s1.122 2018.7

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Fibulin-1の動脈管内膜肥厚形成における役割

中川路太一, 横山詩子, 伊藤智子, 石川義弘

日本病態生理学会雑誌 27 ( 2 ) 40 - 40 2018.7

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胎盤由来プロスタグランディンEはFibulin-1を介した動脈管リモデリングを促進する

横山詩子, 伊藤智子, 石川義弘

日本結合組織学会学術大会プログラム・抄録集 50回 95 - 95 2018.6

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周期加圧培養法による人工血管の作成

石川義弘, 横山詩子, 斎藤純一, 金子真

日本循環制御医学会総会(Web) 39th 22 2018

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The role of tissue plasminogen activator in closure of the ductus arteriosus

横山詩子, 齋藤純一, 石川義弘

日本血栓止血学会誌 29 ( 5 ) 495‐497(J‐STAGE) 2018

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DOI： 10.2491/jjsth.29.495

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2.周期加圧培養法による人工血管の作成

石川義弘, 齋藤純, 横山詩子, 金子真

循環制御(Web) 39 ( 3 ) 155‐156(J‐STAGE) 2018

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DOI： 10.11312/ccm.39.155

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多胎妊娠では動脈管内膜肥厚が抑制される

伊藤智子, 横山詩子, 齋藤純一, 佐藤信一, 臼田治夫, 渡邊真平, 北西龍太, 三浦雄一郎, 埴田卓志, 松田直, 石川義弘

日本新生児成育医学会雑誌 29 ( 3 ) 607 - 607 2017.10

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温熱刺激は、Akt/S6K経路を介して心臓線維芽細胞の活性化を抑制する

成川雅俊, 梅村将就, 木村一雄, 田村功一, 石川義弘

日本心臓病学会学術集会抄録 65回 O - 054 2017.9

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結合組織破壊の分子メカニズムの新展開プロスタグランディンE受容体EP4による弾性線維形成と破壊のメカニズム

横山詩子, 石渡遼, 石川義弘

日本結合組織学会学術大会プログラム・抄録集 49回 50 - 50 2017.6

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Fibulin-1の動脈管内膜肥厚形成機序

伊藤智子, 齋藤純一, 横山詩子, 石川義弘

日本周産期・新生児医学会雑誌 53 ( 2 ) 521 - 521 2017.6

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母体ラットへのベタメタゾン投与が動脈管閉鎖に与える作用の検討

釼持孝博, 横山詩子, 齋藤純一, 伊藤智子, 魚住梓, 岩崎志穂, 西巻滋, 伊藤秀一, 石川義弘

日本周産期・新生児医学会雑誌 53 ( 2 ) 523 - 523 2017.6

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国際的な小児循環器研究を学ぶ午後動脈管の基礎研究から臨床へ

横山詩子, 南沢享, 石川義弘

日本小児科学会雑誌 121 ( 2 ) 196 - 196 2017.2

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Nedd4-2 C2ノックアウトマウスを用いた心房細動の誘発に対する影響の検討

川村飛翔, 峯岸慎太郎, 陳琳, 中島理恵, 木野旅人, 土肥宏志, Prajapati Rajesh, 藤田孝之, 石川義弘, 石上友章

日本内分泌学会雑誌 92 ( 3 ) 904 - 904 2017.1

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ON-CHIP CELL GYM Reviewed

Mitsuhiro Horade, Chia-Hung Dylan Tsai, Hiroaki Ito, Nobuya Higashino, Takayuki Akai, Utako Yokoyama, Yoshihiro Ishikawa, Shinya Sakuma, Fumihito Arai, Makoto Kaneko

30TH IEEE INTERNATIONAL CONFERENCE ON MICRO ELECTRO MECHANICAL SYSTEMS (MEMS 2017) 603 - 604 2017

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DOI： 10.1109/MEMSYS.2017.7863479

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Naチャネル調節因子Nedd4‐2の心臓電気生理学的表現型に与える影響の解析

川村飛翔, 峯岸慎太郎, 中島理恵, 土肥宏志, 陳琳, 木野旅人, 石川義弘, 藤田孝之, PLAJAPATI Rajesh, 石上友章

日本循環器学会関東甲信越地方会(Web) 243rd KANTOKOSHIN'ETSU243,89 (WEB ONLY) 2017

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Fibulin-1は平滑筋細胞遊走を介して動脈管内膜肥厚を誘導する

伊藤智子, 横山詩子, 益田宗孝, 麻生俊英, 石川義弘

日本新生児成育医学会雑誌 28 ( 3 ) 532 - 532 2016.11

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EP4 Signaling in Smooth Muscle Cells Attracts Inflammatory Immune Responses in the Aorta

Ryo Ishiwata, Utako Yokoyama, Yasuhiro Ichikawa, Daisuke Kurotaki, Shota Yasuda, Motohiko Goda, Shinichi Suzuki, Munetaka Masuda, Tomohiko Tamura, Yoshihiro Ishikawa

CIRCULATION 134 2016.11

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Fibulin-1 Plays a Role in Smooth Muscle Cell Migration and Intimal Thickening in the Ductus Arteriosus

Satoko Ito, Utako Yokoyama, Chiharu Yanai, Munetaka Masuda, Toshihide Asou, Yoshihiro Ishikawa

CIRCULATION 134 2016.11

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Functional arterial graft fabricated from pressurized cell-layers

Y. Ishikawa, T. Akimoto, J. Saito, Y. Gonda, S. Sakuma, F. Arai, M. Kaneko, U. Yokoyama

EUROPEAN HEART JOURNAL 37 1404 - 1404 2016.8

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平滑筋細胞におけるPGE2-EP4シグナルは腹部大動脈瘤の発症を促す

石渡遼, 横山詩子, 市川泰広, 黒滝大翼, 田村智彦, 石川義弘

日本循環制御医学会総会プログラム・抄録集 37回 40 - 40 2016.7

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The behavior of cells during Cell Exercise

HIGASHINO Nobuya, KANEKO Makoto, YOKOYAMA Utako, ISHIKAWA Yoshihiro

The Proceedings of JSME annual Conference on Robotics and Mechatronics (Robomec) 2016 ( 0 ) 2A2 - 20a1 2016.6

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When we apply cyclic pressure to smooth muscle cells as if humans do muscle training, the cellular tissue becomes stiffer. We call applying such cyclic pressure to cells in order to make stiff cellular tissue "Cell Exercise". The goal of this study is to understand how cyclic pressure affects cells in microscopic viewpoint. We visualize the behavior of cells under Cell Exercise and under constant pressure, and evaluate the activity of cells with velocity. The transitions of activities have been found different in the two different conditions

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ヒト動脈管における内膜肥厚部の遺伝子プロファイリング

齋藤純一, 横山詩子, 麻生俊英, 石川義弘

日本周産期・新生児医学会雑誌 52 ( 2 ) 546 - 546 2016.6

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Sarcolipinヘテロ欠損マウスにおける心房機能解析

志村大輔, 草刈洋一郎, 笹野哲郎, 中島康弘, 中井岳, 焦其彬, 金美花, 横田知大, 石川義弘, 中野敦, 合田亘人, 南沢享

日本生理学雑誌 78 ( 3 ) 59 - 59 2016.5

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平滑筋細胞におけるPGE2-EP4シグナルは腹部大動脈瘤の慢性炎症をつかさどる

横山詩子, 石渡遼, 石川義弘

日本生理学雑誌 78 ( 3 ) 59 - 59 2016.5

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Magnetized methotrexate for novel anti-cancer therapy

Mayumi Katsumata, Masanari Umemura, Itaru Sato, Makoto Ohtake, Kayoko Oda, Taisuke Akimoto, Rina Nakakaji, Masatoshi Narikawa, Haruki Aoyama, Haruki Eguchi, Yoshihiro Ishikawa

JOURNAL OF PHARMACOLOGICAL SCIENCES 130 ( 3 ) S186 - S186 2016.3

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Magnetized Votrient derivative for novel anti-cancer therapy

Haruki Aoyama, Masanari Umemura, Itaru Sato, Makoto Ohtake, Kayoko Oda, Taisuke Akimoto, Masatoshi Narikawa, Rina Nakakaji, Mayumi Katsumata, Haruki Eguchi, Yoshihiro Ishikawa

JOURNAL OF PHARMACOLOGICAL SCIENCES 130 ( 3 ) S186 - S186 2016.3

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Novel thermo-chemotherapy for oral cancer using a new magnetic anti-cancer drug

I. Sato, M. Umemura, K. Mitsudo, H. Nakashima, M. Kioi, H. Eguchi, M. Ohtake, K. Oda, R. Nakakaji, I. Tohnai, Y. Ishikawa

EUROPEAN JOURNAL OF CANCER 51 S561 - S561 2015.9

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Transient receptor potential cation channel 3 (TRPC3) regulates tumor proliferation and migration of BRAF wild type human malignant melanoma

Kayoko Oda, Masanari Umemura, Mayumi Katsumata, Haruki Aoyama, Ayako Makino, Makoto Ohtake, Itaru Sato, Yukie Yamaguchi, Yoji Nagashima, Michiko Aihara, Yoshihiro Ishikawa, Akane Nagasako

CANCER RESEARCH 75 2015.8

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DOI： 10.1158/1538-7445.AM2015-4371

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Simultaneous hyperthermic-chemotherapy for glioblastoma using a single anti-cancer compound with intrinsic magnetism

Makoto Ohtake, Masanari Umemura, Itaru Sato, Kayoko Oda, Akane Nagasako, Ayako Makino, Haruki Aoyama, Mayumi Katsumata, Haruki Eguchi, Nobutaka Kawahara, Yoshihiro Ishikawa

CANCER RESEARCH 75 2015.8

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DOI： 10.1158/1538-7445.AM2015-4548

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Methotrexate derivative with intrinsic magnetism

Masanari Umemura, Mayumi Katsumata, Itaru Sato, Akane Nagasako, Haruki Aoyama, Ayako Makino, Makoto Ohtake, Kayoko Oda, Kosuke Matsuo, Haruki Eguchi, Yoshihiro Ishikawa

CANCER RESEARCH 75 2015.8

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DOI： 10.1158/1538-7445.AM2015-4398

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ヒト動脈管における内膜肥厚部の遺伝子プロファイリング

齋藤純一, 横山詩子, 市川泰広, 益田宗孝, 麻生俊英, 石川義弘

日本小児循環器学会雑誌 31 ( Suppl.1 ) s1 - 202 2015.7

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未熟児動脈管開存症治療におけるアミノ酸輸液組成の重要性

横山詩子, 藤田秀次郎, 青木理加, 岩崎志穂, 麻生俊英, 益田宗孝, 関和男, 石川義弘

日本小児循環器学会雑誌 31 ( Suppl.1 ) s1 - 324 2015.7

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先天性心疾患の発生と幹細胞医学動脈管分化の分子メカニズム

横山詩子, 矢内千春, 益田宗孝, 麻生俊英, 石川義弘

日本小児循環器学会雑誌 31 ( Suppl.1 ) s1 - 109 2015.7

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ヒト動脈管における内膜肥厚部の遺伝子プロファイリング

齋藤純一, 横山詩子, 市川泰広, 益田宗孝, 麻生俊英, 石川義弘

日本小児循環器学会雑誌 31 ( Suppl.1 ) s1 - 202 2015.7

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未熟児動脈管開存症治療におけるアミノ酸輸液組成の重要性

横山詩子, 藤田秀次郎, 青木理加, 岩崎志穂, 麻生俊英, 益田宗孝, 関和男, 石川義弘

日本小児循環器学会雑誌 31 ( Suppl.1 ) s1 - 324 2015.7

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先天性心疾患の発生と幹細胞医学動脈管分化の分子メカニズム

横山詩子, 矢内千春, 益田宗孝, 麻生俊英, 石川義弘

日本小児循環器学会雑誌 31 ( Suppl.1 ) s1 - 109 2015.7

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心肥大と心不全

石川義弘, 藤田孝之, 梅村将就, 横山詩子

日本病態生理学会雑誌 24 ( 1 ) 28 - 38 2015.5

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Oscillation of cAMP and Ca2+ in cardiac myocytes: a systems biology approach

Takehisa Kamide, Satoshi Okumura, Samik Ghosh, Yoko Shinoda, Yasumasa Mototani, Yoshiki Ohnuki, Huiling Jin, Wenqian Cai, Kenji Suita, Itaru Sato, Masanari Umemura, Takayuki Fujita, Utako Yokoyama, Motohiko Sato, Kazuharu Furutani, Hiroaki Kitano, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 65 ( 2 ) 195 - 200 2015.3

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DOI： 10.1007/s12576-014-0354-3

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Coupling of beta(1)-adrenergic receptor to type 5 adenylyl cyclase and its physiological relevance in cardiac myocytes

Takashi Tsunematsu, Satoshi Okumura, Yasumasa Mototani, Yoshiki Ohnuki, Huiling Jin, Wenqian Cai, Kenji Suita, Itaru Sato, Masanari Umemura, Utako Yokoyama, Motohiko Sato, Takayuki Fujita, Yoshihiro Ishikawa

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 458 ( 3 ) 531 - 535 2015.3

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Myocardial beta-adrenergic receptor (beta-AR) beta(1)- and beta(2)-subtypes are highly homologous, but play opposite roles in cardiac apoptosis and heart failure, as do cardiac adenylyl cyclase (AC) subtypes 5 (AC5) and 6 (AC6): beta(1)-AR and AC5 promote cardiac remodeling, while beta(2)-AR and AC6 activate cell survival pathways. However, the mechanisms involved remain poorly understood. We hypothesized that AC5 is coupled preferentially to beta(1)-AR rather than beta(2)-AR, and we examined this idea by means of pharmacological and genetic approaches. We found that selective inhibition of AC5 with 2'5'-dideoxyadenosine significantly suppressed CAMP accumulation and cardiac apoptosis induced by selective beta(1)-AR stimulation, but had no effect on cAMP accumulation and cardiac apoptosis in response to selective beta(2)-AR stimulation. The results of selective stimulation of beta(1)-AR and beta(2)-AR in neonatal cardiac myocytes prepared from wild-type and AC5-knockout mice were also consistent with the idea that beta(1)-AR selectively couples with AC5. We believe these results are helpful for understanding the mechanisms underlying the different roles of AR subtypes in healthy and diseased hearts. (C) 2015 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.bbrc.2015.01.149

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Coupling of beta(1)-adrenergic receptor to type 5 adenylyl cyclase and its physiological relevance in cardiac myocytes

Takashi Tsunematsu, Satoshi Okumura, Yasumasa Mototani, Yoshiki Ohnuki, Huiling Jin, Wenqian Cai, Kenji Suita, Itaru Sato, Masanari Umemura, Utako Yokoyama, Motohiko Sato, Takayuki Fujita, Yoshihiro Ishikawa

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 458 ( 3 ) 531 - 535 2015.3

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Myocardial beta-adrenergic receptor (beta-AR) beta(1)- and beta(2)-subtypes are highly homologous, but play opposite roles in cardiac apoptosis and heart failure, as do cardiac adenylyl cyclase (AC) subtypes 5 (AC5) and 6 (AC6): beta(1)-AR and AC5 promote cardiac remodeling, while beta(2)-AR and AC6 activate cell survival pathways. However, the mechanisms involved remain poorly understood. We hypothesized that AC5 is coupled preferentially to beta(1)-AR rather than beta(2)-AR, and we examined this idea by means of pharmacological and genetic approaches. We found that selective inhibition of AC5 with 2'5'-dideoxyadenosine significantly suppressed CAMP accumulation and cardiac apoptosis induced by selective beta(1)-AR stimulation, but had no effect on cAMP accumulation and cardiac apoptosis in response to selective beta(2)-AR stimulation. The results of selective stimulation of beta(1)-AR and beta(2)-AR in neonatal cardiac myocytes prepared from wild-type and AC5-knockout mice were also consistent with the idea that beta(1)-AR selectively couples with AC5. We believe these results are helpful for understanding the mechanisms underlying the different roles of AR subtypes in healthy and diseased hearts. (C) 2015 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.bbrc.2015.01.149

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細胞積層法で構築した三次元血管壁モデルを用いた動脈硬化高集積ナノ粒子の創製

松崎典弥, パーニニーチャーパユーン, 横山詩子, 石川義弘, 明石満

再生医療 14 204 2015.2

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組織型プラスミノーゲンアクチベーターによる動脈管閉鎖時の内膜肥厚形成促進作用(Plasminogen activator may promote intimal thickening in the ductus arteriosus)

二町尚樹, 横山詩子, 齋藤純一, 矢内千春, 市川泰広, 益田宗孝, 麻生俊英, 石川義弘

日本小児科学会雑誌 119 ( 2 ) 305 - 305 2015.2

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平滑筋におけるPGE2‐EP4シグナルは腹部大動脈瘤の発症を促進する

石渡遼, 横山詩子, 市川泰弘, 石川義弘

日本薬理学会関東部会プログラム・要旨集 132nd 58 2015

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Role of cyclic AMP sensor Epac1 in masseter muscle hypertrophy and myosin heavy chain transition induced by beta(2)-adrenoceptor stimulation

Yoshiki Ohnuki, Daisuke Umeki, Yasumasa Mototani, Huiling Jin, Wenqian Cai, Kouichi Shiozawa, Kenji Suita, Yasutake Saeki, Takayuki Fujita, Yoshihiro Ishikawa, Satoshi Okumura

JOURNAL OF PHYSIOLOGY-LONDON 592 ( 24 ) 5461 - 5475 2014.12

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DOI： 10.1113/jphysiol.2014.282996

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Decreased serum osmolality promotes ductus arteriosus constriction

Rika Aoki, Utako Yokoyama, Yasuhiro Ichikawa, Masataka Taguri, Shun Kumagaya, Ryo Ishiwata, Chiharu Yanai, Shujiro Fujita, Masanari Umemura, Takayuki Fujita, Satoshi Okumura, Motohiko Sato, Susumu Minamisawa, Toshihide Asou, Munetaka Masuda, Shiho Iwasaki, Shigeru Nishimaki, Kazuo Seki, Shumpei Yokota, Yoshihiro Ishikawa

CARDIOVASCULAR RESEARCH 104 ( 2 ) 326 - 336 2014.11

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DOI： 10.1093/cvr/cvu199

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Development of thermochemotherapy using cisplatin and ferucarbotran (Resovist (R)) in head and neck cancer

Itaru Sato, Masanari Umemura, Kenji Mitsudo, Xianfeng Feng, Hideyuki Nakashima, Mitomu Kioi, Akiyoshi Miyajima, Haruki Eguchi, Iwai Tohnai, Yoshihiro Ishikawa

CANCER RESEARCH 74 ( 19 ) 2014.10

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DOI： 10.1158/1538-7445.AM2014-4576

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A novel treatment for triple-negative breast cancer using intrinsic magnetized paclitaxel

Masanari Umemura, Ayako Makino, Itaru Sato, Xianfeng Feng, Kayoko Oda, Makoto Ohtake, Satoshi Izuka, Maki Iwai, Kosuke Matsuo, Haruki Eguchi, Yoshihiro Ishikawa

CANCER RESEARCH 74 ( 19 ) 2014.10

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DOI： 10.1158/1538-7445.AM2014-5399

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生理機能の理解に基づいた循環器疾患薬物治療の新たな戦略 cAMP標的心血管治療薬

南沢享, 横山詩子, 石川義弘

日本生理学雑誌 76 ( 3 ) 66 - 67 2014.5

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Prostaglandin E-2 receptor EP4 signaling in vascular smooth muscle cells decreases aortic elasticity

Yasuhiro Ichikawa, Utako Yokoyama, Yoshihiro Ishikawa

FASEB JOURNAL 28 ( 1 ) 2014.4

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Balancing GRK2 and EPAC1 levels prevents and relieves chronic pain

Huijing Wang, Cobi J. Heijnen, Cindy T. J. van Velthoven, Hanneke L. D. M. Willemen, Yoshihiro Ishikawa, Xinna Zhang, Anil K. Sood, Anne Vroon, Niels Eijkelkamp, Annemieke Kavelaars

JOURNAL OF CLINICAL INVESTIGATION 123 ( 12 ) 5023 - 5034 2013.12

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DOI： 10.1172/JCI66241

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Decreased Serum Osmolality Augments the Closure of the Ductus Arteriosus in Neonates

Utako Yokoyama, Rika Aoki, Yasuhiro Ichikawa, Shiho Iwasaki, Kazuo Seki, Shigeru Nishimaki, Shumpei Yokota, Susumu Minamisawa, Yoshihiro Ishikawa

CIRCULATION 128 ( 22 ) 2013.11

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Prostaglandin E2 Receptor EP4 Signaling in Vascular Smooth Muscle Decreased Elasticity of the Aorta

Yasuhiro Ichikawa, Utako Yokoyama, Mari Iwamoto, Shumpei Yokota, Susumu Minamisawa, Yoshihiro Ishikawa

CIRCULATION 128 ( 22 ) 2013.11

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【最新生理活性脂質研究-実験手法、基礎的知識とその応用-】 (第4章)臨床編大動脈瘤の進展とPGE2

横山詩子, 石川義弘

遺伝子医学MOOK ( 24 ) 296 - 300 2013.5

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A role for Piezo2 in EPAC1-dependent mechanical allodynia

N. Eijkelkamp, J. E. Linley, J. M. Torres, L. Bee, A. H. Dickenson, M. Gringhuis, M. S. Minett, G. S. Hong, E. Lee, U. Oh, Y. Ishikawa, F. J. Zwartkuis, J. J. Cox, J. N. Wood

NATURE COMMUNICATIONS 4 2013.4

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Development of a novel magnetic anticancer drug for hyperthermic therapy

Masanari Umemura, Hidenobu Fukumura, Itaru Sato, Xianfeng Feng, Haruki Eguchi, Yoshihiro Ishikawa

CANCER RESEARCH 73 ( 8 ) 2013.4

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DOI： 10.1158/1538-7445.AM2013-5567

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Thermochemotherapy with controlled drug delivery using a novel magnetic anti-cancer drug

Itaru Sato, Kenji Mitsudo, Masanari Umemura, Xianfeng Feng, Hidenobu Fukumura, Haruki Eguchi, Hideyuki Nakashima, Mitomu Kioi, Iwai Tohnai, Yoshihiro Ishikawa

CANCER RESEARCH 73 ( 8 ) 2013.4

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DOI： 10.1158/1538-7445.AM2013-5568

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Nuclear Factor kappa B Inhibition Promotes Closure of Rat Ductus Arteriosus

Ichige Kajimura, Utako Yokoyama, Yoshihiro Ishikawa, Susumu Minamisawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S230 - S230 2013

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New strategy of simultaneous hyperthermo-chemotherapy using a novel nano-magnetic anti-cancer drug

Feng Xianfeng, Masanari Umemura, Hidenobu Fukumura, Itaru Sato, Haruki Eguchi, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S225 - S225 2013

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Effects of anti-cancer using a novel magnetic nanoparticle

Itaru Sato, Masanari Umemura, Kenji Mitsudo, Feng Xianfeng, Hitoshi Iizuka, Haruki Eguchi, Iwai Tohnai, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S210 - S210 2013

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Epac1 pathway plays an important role for the development of heart failure through the activation of PKA

Cai Wenqian, Satoshi Okumura, Takayuki Fujita, Jin Meihua, Kenji Suita, Jin Huiling, Yuko Hidaka, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S180 - S180 2013

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The Role of Plasma Hypoosmolarity in Closure of the Ductus Arteriosus

Rika Aoki, Utako Yokoyama, Yasuhiro Ichikawa, Shujiro Fujita, Shun Kumagaya, Shiho Iwasaki, Kazuo Seki, Shigeru Nishimaki, Shumpei Yokota, Susumu Minamisawa, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S175 - S175 2013

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Pharmacological inhibition of STAT 3 protect heart from lipopolysaccharide-induced cardiac dysfunction through the inhibition of Jak2/STAT3/iNOS signaling

Jin Huiling, Satoshi Okumura, Jin Meihua, Cai Wenqian, Kenji Suita, Takashi Tsunematsu, Bai Yunzhe, Takayuki Fujita, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S179 - S179 2013

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TCTP/Fortilin regulates survival of carcinoma cells and cardiomyocytes

Takayuki Fujita, Wenqian Cai, Yuko Hidaka, Huiling Jin, Meihua Jin, Kenji Suita, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S76 - S76 2013

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Epac1 promotes smooth muscle cell migration via calcium/calcineurin-dependent cell polarization

Yuko Kato, Utako Yokoyama, Satoshi Okumura, Susumu Minamisawa, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S199 - S199 2013

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Oxygenation-induced remodeling of postnatal rat ductus arteriosus with basic fibroblast growth factor signaling

Jin Meihua, Utako Yokoyama, Ryo Ishiwata, Susumu Minamisawa, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S51 - S51 2013

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Oscillation model of Ca and cAMP in cardiac myocytes

Takehisa Kamide, Motohiko Sato, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S236 - S236 2013

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Chemotherapeutic and drug delivery systemwith a novel nano-magnetic particle, EI236

Hitoshi Iizuka, Masanari Umemura, Itaru Sato, Feng Xianfeng, Haruki Eguchi, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S225 - S225 2013

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血管弾性線維におけるプロスタグランディンE受容体EP4の役割の検討

ICHIKAWA YASUHIRO, YOKOYAMA UTAKO, MINAMISAWA SUSUMU, ISHIKAWA YOSHIHIRO

日本血管生物医学会学術集会プログラム・抄録集 21st 188 2013

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J-GLOBAL

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Aspartic acid promotes closure of the rat ductus arteriosus

Shujiro Fujita, Utako Yokoyama, Kenji Nagao, Hiroko Jinzu, Rika Aoki, Yasuhiro Ichikawa, Shiho Iwasaki, Shigeru Nishimaki, Kazuo Seki, Shumpei Yokota, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S183 - S183 2013

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Prostaglandin E2 receptor EP4 in coronary smooth muscle cells may play a role in promoting intimal thickening that precedes atherosclerosis

Shun Kumagaya, Utako Yokoyama, Ayami Sato, Kenji Iwai, Hiroshi Nishihara, Takafumi Inoue, Susumu Minamisawa, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S232 - S232 2013

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Mice Overexpressing Prostaglandin E Receptor EP4 in Vascular Smooth Muscle Cells Decreased Elasticity of the Aorta

Yasuhiro Ichikawa, Utako Yokoyama, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S122 - S122 2013

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Vidarabine, an anti-herpesvirus agent, prevents atrial fibrillation in mice

Kenji Suite, Cai Wenqian, Jin Huiling, Jin Meihua, Takayuki Fujita, Satoshi Okumura, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S120 - S120 2013

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Cross-communication between the L-type Ca2+ channel and beta - adrenergic receptor/adenylyl cyclase/cAMP pathway in mouse ventricular myocytes

Satomi Adachi-Akahane, Izumi-Hiroko Nakaseko, Atsushi Sugiyama, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S132 - S132 2013

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The function of Store-operated Ca2+ entry(SOCE)in melanoma

Masanari Umemura, Takayuki Fujita, Utako Yokoyama, Yoshihiro Ishikawa, Kousaku Iwatsubo

JOURNAL OF PHYSIOLOGICAL SCIENCES 63 S74 - S74 2013

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Disruption of Epaci Decreases Phosphorylation of Phospholamban and Protects the Heart Against Stresses

Satoshi Okumura, Meihua Jin, Yoshiki Ohnuki, Iyuki Namekata, Reiko Kurotani, Takayuki Fujita, Hui-Ling Jin, Weniqian Cai, Yunzhe Bai, Kenji Suita, Takashi Tsunematsu, Hikaru Tanaka, Yoshihiro Ishikawa

CIRCULATION 126 ( 21 ) 2012.11

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Inhibition of Phosphodiesterase Type 3 Dilates the Rat Ductus Arteriosus Without Inducing Intimal Thickening and Respiratory Distress

Yasuhiro Ichikawa, Utako Yokoyama, Mari Iwamoto, Munetaka Masuda, Toshihide Asou, Yoshihiro Ishikawa

CIRCULATION 126 ( 21 ) 2012.11

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Inhibition of Phosphodiesterase Type 3 Dilates the Rat Ductus Arteriosus Without Inducing Intimal Thickening

Yasuhiro Ichikawa, Utako Yokoyama, Mari Iwamoto, Jin Oshikawa, Satoshi Okumura, Motohiko Sato, Shumpei Yokota, Munetaka Masuda, Toshihide Asou, Yoshihiro Ishikawa

CIRCULATION JOURNAL 76 ( 10 ) 2456 - 2464 2012.10

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新たな技術で探る血管構築から機能獲得へのメカニズム血管の弾性機能制御の分子メカニズム

横山詩子, 塩田亜樹, 石渡遼, 鈴木伸一, 益田宗孝, 麻生俊英, 青木浩樹, 杉本幸彦, 中邨智之, 南沢享, 石川義弘

日本生理学雑誌 74 ( 5 ) 253 - 253 2012.9

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Plasma Hypoosmolarity After Birth Promotes Closure of the Ductus Arteriosus

Rika Aoki, Utako Yokoyama, Yasuhiro Ichikawa, Shun Kumagaya, Shiho Iwasaki, Shigeru Nishimaki, Kazuo Seki, Shumpei Yokota, Susumu Minamisawa, Yoshihiro Ishikawa

CIRCULATION RESEARCH 111 ( 4 ) 2012.8

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アミノ酸輸液の組成の違いが動脈管閉鎖に及ぼす作用の検討

FUJITA SHUJIRO, YOKOYAMA UTAKO, AOKI RIKA, OGO HIROSHI, IWASAKI SHIHO, NISHIMAKI SHIGERU, SEKI KAZUO, YOKOTA SHUMPEI, ISHIKAWA YOSHIHIRO

日本周産期・新生児医学会雑誌 48 ( 2 ) 491 - 491 2012.6

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ラット動脈管リモデリングにおけるprostaglandin E2-Nuclear Factor kappa B経路の活性化

梶村いちげ, 横山詩子, 石川義弘, 南沢享

日本小児循環器学会雑誌 28 ( Suppl. ) s213 - s213 2012.6

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Prevention of heart failure in mice by an antiviral agent that inhibits type 5 cardiac adenylyl cyclase

Kosaku Iwatsubo, Claudio Bravo, Masami Uechi, Erdene Baljinnyam, Takashi Nakamura, Masanari Umemura, Lo Lai, Shumin Gao, Lin Yan, Xin Zhao, Misun Park, Hongyu Qiu, Satoshi Okumura, Mizuka Iwatsubo, Dorothy E. Vatner, Stephen F. Vatner, Yoshihiro Ishikawa

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY 302 ( 12 ) H2622 - H2628 2012.6

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出生後の肺における弾性線維形成の発達の検討

市川泰広, 横山詩子, 岩本眞理, 南沢享, 石川義弘

日本小児循環器学会雑誌 28 ( Suppl. ) s212 - s212 2012.6

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Inhibition of EP4 Signaling Attenuates Aortic Aneurysm Formation

Utako Yokoyama, Ryo Ishiwata, Mei-Hua Jin, Yuko Kato, Orie Suzuki, Huiling Jin, Yasuhiro Ichikawa, Syun Kumagaya, Yuzo Katayama, Takayuki Fujita, Satoshi Okumura, Motohiko Sato, Yukihiko Sugimoto, Hiroki Aoki, Shinichi Suzuki, Munetaka Masuda, Susumu Minamisawa, Yoshihiro Ishikawa

PLOS ONE 7 ( 5 ) 2012.5

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Acute myocardial infarction with isolated conus branch occlusion

Masanari Umemura, David Ho, Naoki Nozawa, Erdene Balginnyam, Kousaku Iwatsubo, Thosihiko Saito, Tsutomu Endo, Yoshihiro Ishikawa, Satoshi Umemura, Kazuo Kimura

JOURNAL OF ELECTROCARDIOLOGY 45 ( 3 ) 285 - 287 2012.5

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DOI： 10.1016/j.jelectrocard.2011.11.006

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Effect of ascorbic acid on reactive oxygen species production in chemotherapy and hyperthermia in prostate cancer cells

Hidenobu Fukumura, Motohiko Sato, Kyouhei Kezuka, Itaru Sato, Xianfeng Feng, Satoshi Okumura, Takayuki Fujita, Utako Yokoyama, Haruki Eguchi, Yoshihiro Ishikawa, Tomoyuki Saito

JOURNAL OF PHYSIOLOGICAL SCIENCES 62 ( 3 ) 251 - 257 2012.5

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DOI： 10.1007/s12576-012-0204-0

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Mice Lacking Hypertension Candidate Gene ATP2B1 in Vascular Smooth Muscle Cells Show Significant Blood Pressure Elevation

Yusuke Kobayashi, Nobuhito Hirawa, Yasuharu Tabara, Hidenori Muraoka, Megumi Fujita, Nobuko Miyazaki, Akira Fujiwara, Yasuhiro Ichikawa, Yuichiro Yamamoto, Naoaki Ichihara, Sanae Saka, Hiromichi Wakui, Shin-ichiro Yoshida, Keisuke Yatsu, Yoshiyuki Toya, Gen Yasuda, Katsuhiko Kohara, Yoshikuni Kita, Kohtaro Takei, Yoshio Goshima, Yoshihiro Ishikawa, Hirotsugu Ueshima, Tetsuro Miki, Satoshi Umemura

HYPERTENSION 59 ( 4 ) 854 - U213 2012.4

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DOI： 10.1161/HYPERTENSIONAHA.110.165068

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大動脈瘤形成におけるプロスタグランディンE受容体EP4の役割の検討

片山雄三, 横山詩子, 根本寛子, 笠間啓一郎, 鈴木伸一, 磯松幸尚, 内田敬二, 井元清隆, 石川義弘, 益田宗孝

日本心臓血管外科学会雑誌 41 ( Suppl. ) 489 - 489 2012.3

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Acute pulmonary embolism induced by renal obstruction with benign prostatic hyperplasia: Case report

Masanari Umemura, David Ho, Naoki Nozawa, Erdene Balginnyam, Kousaku Iwatsubo, Toshihiko Saito, Tsutomu Endo, Yoshihiro Ishikawa, Satoshi Umemura, Kazuo Kimura

Journal of Cardiology Cases 5 ( 1 ) e39 - e43 2012.2

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DOI： 10.1016/j.jccase.2011.10.004

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Sarcalumenin plays a critical role in age-related cardiac dysfunction due to decreases in SERCA2a expression and activity

Qibin Jiao, Hiroshi Takeshima, Yoshihiro Ishikawa, Susumu Minamisawa

CELL CALCIUM 51 ( 1 ) 31 - 39 2012.1

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DOI： 10.1016/j.ceca.2011.10.003

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Morphological and Histological Evaluations of 3D-Layered Blood Vessel Constructs Prepared by Hierarchical Cell Manipulation

Michiya Matsusaki, Koji Kadowaki, Eijiro Adachi, Takeshi Sakura, Utako Yokoyama, Yoshihiro Ishikawa, Mitsuru Akashi

JOURNAL OF BIOMATERIALS SCIENCE-POLYMER EDITION 23 ( 1-4 ) 63 - 79 2012

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DOI： 10.1163/092050610X541953

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Pharmacological intervention of Gbetagamma signal mediated by Activator of G-protein signaling 8 in the cardiomyocytes under hypoxia.

Motohiko Sato, Masahiro Hiraoka, Yukiko Yamane, Xianfeng Feng, Yoshihiro Ishikawa

JOURNAL OF PHARMACOLOGICAL SCIENCES 118 198P - 198P 2012

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Epac Activation Protects Heart From Interleukin-6-Induced Cardiac Dysfunction by Inhibiting Stat/iNOS Signaling

Satoshi Okumura, Meihua Jin, Fumika Kawamata, Hui-Ling Jin, Wenqian Cai, Yunzhe Bai, Kenji Suita, Yuko Hidaka, Takashi Tsunematsu, Yoshihiro Ishikawa

CIRCULATION 124 ( 21 ) 2011.11

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Cardiac Protection From Hypoxic Injury by a Novel Synthetic Peptide Targeting the Activator of G-Protein Signaling 8-Mediated G beta gamma Signal

Motohiko Sato, Masahiro Hiraoka, Yukiko Yamane, Feng Xianfeng, Yoshihiro Ishikawa

CIRCULATION 124 ( 21 ) 2011.11

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Inhibition of Adenylyl Cyclase Type 5 Protects Against Obesity and Diabetes

David Ho, Lin Yan, Xin Zhao, Shumin Gao, Kousaku Iwatsubo, Yoshihiro Ishikawa, Dorothy E. Vatner, Stephen F. Vatner

CIRCULATION 124 ( 21 ) 2011.11

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動脈管収縮における出生後の血清浸透圧低下の役割

青木理加, 横山詩子, 岩崎志穂, 堀口晴子, 関和男, 西巻滋, 横田俊平, 石川義弘

日本未熟児新生児学会雑誌 23 ( 3 ) 551 - 551 2011.10

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Apoptosis in Heart Failure - The Role of the beta-Adrenergic Receptor-Mediated Signaling Pathway and p53-Mediated Signaling Pathway in the Apoptosis of Cardiomyocytes

Takayuki Fujita, Yoshihiro Ishikawa

CIRCULATION JOURNAL 75 ( 8 ) 1811 - 1818 2011.8

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DOI： 10.1253/circj.CJ-11-0025

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cAMPシグナルを標的にしたヒアルロン酸産生制御メカニズムの研究

石川義弘, 横山詩子

コスメトロジー研究報告 19 91 - 95 2011.8

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Y1-2 Epac1は血管障害時の内膜肥厚形成を促進する(優秀演題賞候補口演1,第53回日本平滑筋学会総会)

加藤優子, 横山詩子, 奥村敏, 南沢享, 佐田政隆, 宮島栄治, 石川義弘

日本平滑筋学会雑誌 15 ( 1 ) "J - 15" 2011.7

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Epac1は血管障害時の内膜肥厚形成を促進する

加藤優子, 横山詩子, 奥村敏, 南沢享, 佐田政隆, 宮島栄治, 石川義弘

日本平滑筋学会雑誌 15 ( 1 ) J - 15 2011.7

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Secretoglobin 3A2 Suppresses Bleomycin-induced Pulmonary Fibrosis by Transforming Growth Factor beta Signaling Down-regulation

Reiko Kurotani, Satoshi Okumura, Tsutomu Matsubara, Utako Yokoyama, John R. Buckley, Takeshi Tomita, Kyohei Kezuka, Tomokazu Nagano, Dominic Esposito, Troy E. Taylor, William K. Gillette, Yoshihiro Ishikawa, Hiroyuki Abe, Jerrold M. Ward, Shioko Kimura

JOURNAL OF BIOLOGICAL CHEMISTRY 286 ( 22 ) 19682 - 19692 2011.6

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DOI： 10.1074/jbc.M111.239046

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出生後の血清浸透圧低下は動脈管収縮を促進させる

市川泰広, 青木理加, 横山詩子, 岩本眞理, 南沢享, 石川義弘

日本小児循環器学会雑誌 27 ( Suppl. ) s303 - s303 2011.6

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Identification of Transcription Factor E3 (TFE3) as a Receptor-independent Activator of G alpha(16) GENE REGULATION BY NUCLEAR G alpha SUBUNIT AND ITS ACTIVATOR

Motohiko Sato, Masahiro Hiraoka, Hiroko Suzuki, Yunzhe Bai, Reiko Kurotani, Utako Yokoyama, Satoshi Okumura, Mary J. Cismowski, Stephen M. Lanier, Yoshihiro Ishikawa

JOURNAL OF BIOLOGICAL CHEMISTRY 286 ( 20 ) 17766 - 17776 2011.5

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DOI： 10.1074/jbc.M111.219816

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DNA microarray profiling identified a new role of growth hormone in vascular remodeling of rat ductus arteriosus

Mei-Hua Jin, Utako Yokoyama, Yoji Sato, Aki Shioda, Qibin Jiao, Yoshihiro Ishikawa, Susumu Minamisawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 61 ( 3 ) 167 - 179 2011.5

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DOI： 10.1007/s12576-011-0133-3

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Cardiac Overexpression of Adenylyl Cyclase Type 5 Induces Left Ventricular Hypertrophy Potentially by Activating Calcineurin-NFAT Signaling

Misun Park, Ji Yeon Park, Jung Ah Lee, Bin Tian, Lo Lai, Kosaku Iwatsubo, Yoshihiro Ishikawa, Junichi Sadoshima, Dorothy E. Vatner, Stephen F. Vatner

FASEB JOURNAL 25 2011.4

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Novel Activator of G-protein signaling 11 (AGS11)/TFE3 regulates transcription of claudin via activation of nuclear Galpha16

Motohiko Sato, Masahiro Hiraoka, Hiroko Suzuki, Yunzhe Bai, Satoshi Okumura, Yoshihiro Ishikawa

JOURNAL OF PHARMACOLOGICAL SCIENCES 115 90P - 90P 2011

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プロスタグランディンE受容体EP4シグナルによる弾性線維形成の制御

塩田亜樹, 横山詩子, 加藤優子, 麻生俊英, 青木浩樹, 中邨智之, 南沢亨, 石川義弘

日本生化学会大会・日本分子生物学会年会合同大会講演要旨集 83回・33回 2P - 0266 2010.12

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Overexpression of Adenylyl Cyclase Type 5 (AC5) in the Heart Predisposes to Cardiac Arrhythmias

Zhenghang Zhao, Gopal J. Babu, Nadezhda Fefelova, Yoshihiro Ishikawa, Kousaku Iwatsubo, Lo Lai, Lin Yan, Dorothy E. Vatner, Stephen F. Vatner, Lai-Hua Xie

CIRCULATION 122 ( 21 ) 2010.11

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Heart Failure Rescued by Pharmacological Inhibition of Type 5 Adenylyl Cyclase

Kosaku Iwatsubo, Erdene Baljinnyam, Lo Lai, Chull Hong, Shumin Gao, Lin Yan, Dorothy Vatner, Junichi Sadoshima, Stephen Vatner, Yoshihiro Ishikawa

CIRCULATION 122 ( 21 ) 2010.11

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Novel Transcription Regulation in the Hypertrophied Myocardium via Nuclear Galpha16 Subunit and Activator of G-Protein Signaling (AGS)

Motohiko Sato, Masaharu Hiraoka, Hiroko Suzuki, Yunzhe Bai, Satoshi Okumura, Mary J. Cismowski, Stephen M. Lanier, Yoshihiro Ishikawa

CIRCULATION 122 ( 21 ) 2010.11

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ラット動脈管閉鎖における低浸透圧センサーTransient Receptor Potential Melastatin 3(TRPM3)チャネルの役割

青木理加, 横山詩子, 岩崎志穂, 西巻滋, 横田俊平, 石川義弘

日本未熟児新生児学会雑誌 22 ( 3 ) 521 - 521 2010.10

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Effects of cardiac overexpression of type 6 adenylyl cyclase affects on the response to chronic pressure overload

Aziz Guellich, Shumin Gao, Chull Hong, Lin Yan, Thomas E. Wagner, Sunil K. Dhar, Bijan Ghaleh, Luc Hittinger, Kosaku Iwatsubo, Yoshihiro Ishikawa, Stephen F. Vatner, Dorothy E. Vatner

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY 299 ( 3 ) H707 - H712 2010.9

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DOI： 10.1152/ajpheart.00148.2010

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Differential Roles of Epac in Regulating Cell Death in Neuronal and Myocardial Cells

Sayaka Suzuki, Utako Yokoyama, Takaya Abe, Hiroshi Kiyonari, Naoya Yamashita, Yuko Kato, Reiko Kurotani, Motohiko Sato, Satoshi Okumura, Yoshihiro Ishikawa

JOURNAL OF BIOLOGICAL CHEMISTRY 285 ( 31 ) 24248 - 24259 2010.7

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DOI： 10.1074/jbc.M109.094581

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Prostaglandin E2-activated Epac promotes neointimal formation of the rat ductus arteriosus by a process distinct from that of cAMP-dependent protein kinase A(Special lecture, 52^<nd> Annual Meeting of the Japan Society of Smooth Muscle Research)

横山詩子, 南沢享, 石川義弘

Nihon heikatsukin gakkaizassi 14 ( 1 ) "J - 4" 2010.6

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DOI： 10.1540/heikatsukinzashi.14.J4

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Differential Regulation of Vascular Tone and Remodeling via Stimulation of Type 2 and Type 6 Adenylyl Cyclases in the Ductus Arteriosus

Utako Yokoyama, Susumu Minamisawa, Ayako Katayama, Tong Tang, Sayaka Suzuki, Kousaku Iwatsubo, Shiho Iwasaki, Reiko Kurotani, Satoshi Okumura, Motohiko Sato, Shumpei Yokota, H. Kirk Hammond, Yoshihiro Ishikawa

CIRCULATION RESEARCH 106 ( 12 ) 1882 - U232 2010.6

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DOI： 10.1161/CIRCRESAHA.109.214924

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Regulation of vascular tone and remodeling of the ductus arteriosus

Utako Yokoyama, Susumu Minamisawa, Yoshihiro Ishikawa

Journal of Smooth Muscle Research 46 ( 2 ) 77 - 87 2010.6

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DOI： 10.1540/jsmr.46.77

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プロスタグランディンE2-Epacシグナルによるラット動脈管の内膜肥厚形成の促進作用

横山詩子, 南沢享, 石川義弘

日本平滑筋学会雑誌 14 ( 1 ) J - 4 2010.6

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Down-regulation of MnSOD via Sirt1/FoxO3a complex increase oxidative stress with cardiac overexpression of Type 5 Adenylyl Cyclase

Lo Lai, Lin Yan, Che-Lin Hu, Shumin Gao, Kosaku Iwatsubo, Yoshihiro Ishikawa, Junichi Sadoshima, Stephen F. Vatner, Dorothy E. Vatner

FASEB JOURNAL 24 2010.4

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Microarray Analysis Provides a Link between Adenylyl Cyclase Type 5 and Pressure Overload Hypertrophy

Misun Park, Ji Yeon Park, Bin Tian, Lin Yan, Lo Lai, Hongyu Qiu, Aziz Guellich, Kosaku Iwatsubo, Yoshihiro Ishikawa, Junichi Sadoshima, Dorothy E. Vatner, Stephen F. Vatner

FASEB JOURNAL 24 2010.4

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HIPPA : 個人情報保護の厳格化(用語解説)

石川義弘

循環器専門医 : 日本循環器学会専門医誌 18 ( 1 ) 67 - 67 2010.3

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SIMCOR(高脂血症治療の合剤薬) : 合剤の多様化(用語解説)

石川義弘

循環器専門医 : 日本循環器学会専門医誌 18 ( 1 ) 106 - 106 2010.3

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ラノラジン : 10年ぶりの狭心症治療薬(用語解説)

石川義弘

循環器専門医 : 日本循環器学会専門医誌 18 ( 1 ) 150 - 150 2010.3

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A molecular dissociation between cued and contextual appetitive learning

Mazen A. Kheirbek, Jeff A. Beeler, Wanhao Chi, Yoshihiro Ishikawa, Xiaoxi Zhuang

LEARNING & MEMORY 17 ( 3 ) 148 - 154 2010.3

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DOI： 10.1101/lm.1687310

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ラット動脈管リモデリングにおけるbFGFの役割(The Role of bFGF in Vascular Remodeling in Rat Ductus Arteriosus)

金美花, 横山詩子, 赤池徹, 青木理加, 焦其彬, 横田俊平, 南沢享, 石川義弘

日本小児科学会雑誌 114 ( 2 ) 342 - 342 2010.2

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Sarcalumenin plays a critical role in age-related cardiac dysfunction due to decreases in SERCA2a expression and activity

Qibin Jiao, Toru Akaike, Hiroshi Takeshima, Yoshihiro Ishikawa, Susumu Minamisawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 60 S94 - S94 2010

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Regulation of connexin 43 by activator of G protein signaling 8 and G beta gamma

Motohiko Sato, Masahiro Hiraoka, Qibin Jiao, Hiroko Suzuki, Reiko Kurotani, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 60 S77 - S77 2010

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Sarcalumenin Plays a Critical Role in Age-related Cardiac Dysfunction due to Decreases in SERCA2a Expression and Activity

JIAO Qibin, AKAIKE Toru, TAKESHIMA Hiroshi, ISHIKAWA Yoshihiro, MINAMISAWA Susumu

Circulation Journal 74 ( Supplement 1 ) 2010

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Connexin 43 was regulated by Ischemia-inducible G-protein activator and G beta gamma under hypoxic stress

Motohiko Sato, Masahiro Hiraoka, Qibin Jiao, Hiroko Suzuki, Reiko Kurotani, Stephen M. Lanier, Yoshihiro Ishikawa

JOURNAL OF PHARMACOLOGICAL SCIENCES 112 151P - 151P 2010

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SCGB3A2 suppresses bleomycin-induced lung fibrosis through activation of STAT1

Reikol Kurotani, Kyohei Kezuka, Shioko Kimura, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 60 S197 - S197 2010

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Inhibition of specific adenylyl cyclase isoforms by lithium and carbamazepine, but not valproate, may be related to their antidepressant effect

Liad Mann, Eliahu Heldman, Yuly Bersudsky, Stephen F. Vatner, Yoshihiro Ishikawa, Orna Almog, Robert H. Belmaker, Galila Agam

BIPOLAR DISORDERS 11 ( 8 ) 885 - 896 2009.12

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DOI： 10.1111/j.1399-5618.2009.00762.x

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Adenylyl cyclase type 5 protein expression during cardiac development and stress

Che-Lin Hu, Rachna Chandra, Hui Ge, Jayashree Pain, Lin Yan, Gopal Babu, Christophe Depre, Kousaku Iwatsubo, Yoshihiro Ishikawa, Junichi Sadoshima, Stephen F. Vatner, Dorothy E. Vatner

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY 297 ( 5 ) H1776 - H1782 2009.11

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DOI： 10.1152/ajpheart.00050.2009

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Roles of Ischemia-inducible G-protein Activator in Hypoxia-Induced Apoptosis of Cardiomyocytes and Its Regulation of Connexin 43

Motohiko Sato, Qibin Jiao, Masahiro Hiraoka, Reiko Kurotani, Eiji Toyota, Stephen M. Lanier, Yoshihiro Ishikawa

CIRCULATION 120 ( 18 ) S1167 - S1167 2009.11

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Epac in melanoma: a contributor to tumor cell physiology? Focus on "Epac increases melanoma cell migration by a heparin sulfate-related mechanism"

Frank Lezoualc'h

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY 297 ( 4 ) C797 - C799 2009.10

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DOI： 10.1152/ajpcell.00358.2009

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胎生後期ラット動脈管におけるTRPMチャネルの発現大動脈組織との比較検討

青木理加, 横山詩子, 岩崎志穂, 西巻滋, 横田俊平, 石川義弘

日本未熟児新生児学会雑誌 21 ( 3 ) 506 - 506 2009.10

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Adenylyl Cyclase Type 5 Contributes to Corticostriatal Plasticity and Striatum-Dependent Learning

Mazen A. Kheirbek, Jon P. Britt, Jeff A. Beeler, Yoshihiro Ishikawa, Daniel S. McGehee, Xiaoxi Zhuang

JOURNAL OF NEUROSCIENCE 29 ( 39 ) 12115 - 12124 2009.9

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DOI： 10.1523/JNEUROSCI.3343-09.2009

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Epac enhances melanoma cell migration through tubulin polymerization

Erdene Baljinnyam, Yoshihiro Ishikawa, Mizuka Iwatsubo, Kosaku Iwatsubo

CANCER RESEARCH 69 2009.5

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Epac increases melanoma cell migration via intracellular Ca2+release from endoplasmic reticulum

Erdene Baljinnyam, Yoshihiro Ishikawa, Martha Nowycky, Mizuka Iwatsubo, Kosaku Iwatsubo

CANCER RESEARCH 69 2009.5

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The Level of Cardiac Specific Overexpression of Adenylyl Cyclase Type 2 Dictates the Response to Chronic Pressure Overload

Aziz Guellich, Che-Lin Hu, Lin Yan, Chull Hong, Shumin Gao, Luke F. Fritzky, Thomas Wagner, Yoshihiro Ishikawa, Kosaku Iwatsubo, Luc Hittinger, Bijan Ghaleh, Junichi Sadoshima, Dorothy E. Vatner, Stephen F. Vatner

FASEB JOURNAL 23 2009.4

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PE-063 Oxygenation Promotes Calcium-dependent Smooth Muscle Cell Migration in the Rat Ductus Arteriosus(PE011,Congenital Heart Disease (M),Poster Session (English),The 73rd Annual Scientific Meeting of The Japanese Circulation Society)

Akaike Toru, Yokoyama Utako, Iwamoto Mari, Ishikawa Yoshihiro, Minamisawa Susumu

Circulation journal : official journal of the Japanese Circulation Society 73 414 - 414 2009.3

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FRS-074 Activation of Epac1-specific Signaling Protects Heart from Cytokine-mediated Cardiac Dysfunction through the Inhibition of Proinflamatory Cytokine Signaling(FRS15,Novel Molecular Mechanisms of Heart Failure 1 (M),Featured Research Session (English),The 73rd Annual Scientific Meeting of The Japanese Circulation Society)

Okumura Satoshi, Suzuki Sayaka, Bai Yunzhe, Jin Meihua, Hidaka Yuko, Kurotani Reiko, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 73 156 - 156 2009.3

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OE-319 Adenylyl Cyclase Type 6, but not Type 2 and 5, Selectively Promotes cAMP-dependent Vascular Remodeling in Rat Ductus Arteriosus(OE54,Congenital Heart Disease/Kawasaki's Disease (M),Oral Presentation (English),The 73rd Annual Scientific Meeting of The Japanese Circulation Society)

Yokoyama Utako, Minamisawa Susumu, Katayama Ayako, Akaike Toru, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 73 255 - 255 2009.3

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Adenylyl Cyclase Type 5 Disruption Prolongs Longevity and Protects the Heart Against Stress

Stephen F. Vatner, Lin Yan, Yoshihiro Ishikawa, Dorothy E. Vatner, Junichi Sadoshima

CIRCULATION JOURNAL 73 ( 2 ) 195 - 200 2009.2

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DOI： 10.1253/circj.CJ-08-0957

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ALTERATIONS OF CARDIAC CONNEXIN 43 UNDER HYPOXIC STRESS: ROLES OF ACTIVATOR OF G PROTEIN SIGNALING 8 AND G-beta gamma

Jiao Qibin, Motohiko Sato, Hiroko Suzuki, Reiko Kurotani, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 59 158 - 158 2009

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REQUIREMENT OF RECEPTOR-INDEPENDENT G-PROTEIN ACTIVATOR, ACTIVATOR OF G PROTEIN SIGNALING 8 FOR HYPOXIA-INDUCED APOPTOSIS OF CARDIOMYOCYTES

Motohiko Sato, Takashi Honda, Qibin Jiao, Reiko Kurotani, Eiji Toyota, Stephen M. Lanier, Yoshihiro Ishikawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 59 159 - 159 2009

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An involvement of Activator of G-protein Signaling 8 (AGS8) in hypoxia-induced apoptosis of cardiomyocytes

Motohiko Sato, Takashi Honda, Qibin Jiao, Reiko Kurotani, Eiji Toyota, Stephen M. Lanier, Yoshihiro Ishikawa

JOURNAL OF PHARMACOLOGICAL SCIENCES 109 265P - 265P 2009

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Cardiac-Specific Overexpression of Caveolin-3 Induces Endogenous Cardiac Protection by Mimicking Ischemic Preconditioning

Yasuo M. Tsutsumi, Yousuke T. Horikawa, Michelle M. Jennings, Michael W. Kidd, Ingrid R. Niesman, Utako Yokoyama, Brian P. Head, Yasuko Hagiwara, Yoshihiro Ishikawa, Atsushi Miyanohara, Piyush M. Patel, Paul A. Insel, Hemal H. Patel, David M. Roth

CIRCULATION 118 ( 19 ) 1979 - 1988 2008.11

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DOI： 10.1161/CIRCULATIONAHA.108.788331

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A cAMP Pathway Underlying Reward Prediction in Associative Learning

Mazen A. Kheirbek, Jeff A. Beeler, Yoshihiro Ishikawa, Xiaoxi Zhuang

JOURNAL OF NEUROSCIENCE 28 ( 44 ) 11401 - 11408 2008.10

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DOI： 10.1523/JNEUROSCI.4115-08.2008

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Activation of Epaci-Specific Signaling Protects Heart from Cytokine-Mediated Cardiac Dysfunction through the Inhibition of Proinflamatory Cytokine Signaling

Satoshi Okumura, Sayaka Suzuki, Bai Yunzhe, Meihua Jin, Relko Kurotani, Yoshihiro Ishikawa

CIRCULATION 118 ( 18 ) S385 - S385 2008.10

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The Role For Caveolin And Caveolae In Delayed Protection From Ischemia-reperfusion Injury

Yasuo M. Tsutsumi, Blake Chin-Lee, Yoshihiro Ishikawa, David M. Roth, Hemal H. Patel

CIRCULATION 118 ( 18 ) S358 - S358 2008.10

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An Involvement of a Novel G-protein Activator on Hypoxia-Induced Apoptosis of Cardiomyocytes and its Interaction with Connexin 43

Motohiko Sato, Takashi Honda, Qibin Jiao, Reiko Kurotani, Eiji Toyota, Stephen M. Lanier, Yoshihiro Ishikawa

CIRCULATION 118 ( 18 ) S486 - S486 2008.10

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Pharmacological Inhibition of Type 5 Adenylyl Cyclase Attenuates Functional Deterioration in Chronic Catecholamine Stress

Kosaku Iwatsubo, Erdene Baljinnyam, Shumin Gao, Junichi Sadoshima, Dorothy E. Vatner, Stephen F. Vatner, Yoshihiro Ishikawa

CIRCULATION 118 ( 18 ) S542 - S542 2008.10

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サイクリックAMPによる心臓線維芽細胞を標的とした心臓線維化治療の検討

横山詩子, Paul Insel, 石川義弘

日本内分泌学会雑誌 84 ( 2 ) 685 - 685 2008.9

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動脈管におけるT型カルシウムチャンネルの役割

赤池徹, 横山詩子, 全紅, 岩本眞理, 石川義弘, 南沢享

日本小児循環器学会雑誌 24 ( 4 ) 568 - 568 2008.7

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動脈管閉鎖内膜肥厚の分子機序解明―新たな動脈管開存症の治療法開発をめざして―

南沢享, 横山詩子, 石川義弘, 赤池徹, 岩崎志穂

母子健康協会小児医学助成研究報告書 19th 19 - 21 2008.6

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Apelin-APJ system plays an important role in preventing catecholamine-induced cardiac hypertrophy

N. Ichihara, S. Minamisawa, T. Hashimoto, K. Uchino, A. Fukamizu, Y. Ishikawa, S. Umemura

JOURNAL OF HYPERTENSION 26 S263 - S263 2008.6

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Apelin-APJ系はカテコラミン誘発性心肥大を防止する上で重要な役割を持つ

一原直昭, 橋本達夫, 内野和顕, 深水昭吉, 南沢享, 石川義弘, 梅村敏

循環制御 29 ( Suppl. ) 84 - 84 2008.5

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An improved technique for esophagojejunostomy with a novel anvil after total gastrectomy grasping forceps

Akio Ashida, Hiroshi Matsukawa, Joji Samejima, Keita Fujii, Hiroyuki Adachi, Yoshihiro Ishikawa, Naoto Kato, Jun Fujisawa, Yasushi Rino, Toshio Imada

JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS 206 ( 4 ) 754 - 755 2008.4

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DOI： 10.1016/j.jamcollsurg.2007.08.006

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T-type calcium channels regulate smooth muscle cell migration, neointimal formation, and oxygen-induced vascular contraction in rat ductus arteriosus

Toru Akaike, Utako Yokoyama, Hong Quan, Yoshihiro Ishikawa, Susumu Minamisawa

FASEB JOURNAL 22 2008.4

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Epac1, an exchange protein activated by cAMP, increases cell migration through syndecan clustering. PI3K activation and heparan sulphate production

Erdene Baljinnyam, Kousaku Iwatsubo, Xu Wang, Coskun Ulucan, David Lagunoff, Yoshihiro Ishikawa

FASEB JOURNAL 22 2008.4

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Sarcalumenin plays a critical role in age-dependent reduction in cardiac function and SERCA2a activity

Qibin Jiao, Miei Shimura, Toru Akaike, Yoshihiro Ishikawa, Susumu Minamisawa

FASEB JOURNAL 22 2008.4

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PJ-432 Rising Oxygen Tension Promoted Smooth Muscle Cell Migration in the Rat Ductus Arteriosus(Congenital heart disease/Kawasaki's disease(02)(M),Poster Session(Japanese),The 72nd Annual Scientific Meeting of the Japanese Circulation Society)

Akaike Toru, Yokoyama Utako, Iwamoto Mari, Satoh Motohiko, Ishikawa Yoshihiro, Minamisawa Susumu

Circulation journal : official journal of the Japanese Circulation Society 72 621 - 621 2008.3

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OE-078 Cardiac Overexpression of Epac1 in Transgenic Mice Protects Heart from Lipopolysaccharide-induced Cardiac Dysfunction and inhibits JAK-STAT pathway(Heart failure, basic(01)(M),Oral Presentation(English),The 72nd Annual Scientific Meeting of the Japanese Circulation Society)

Okumura Satoshi, Yunzhe Bai, Meihua Jin, Kurotani Reiko, Iwatsubo Kosaku, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 72 199 - 200 2008.3

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Adenylyl Cyclase Type 5 Disruption Prolongs Longevity and Protects the Heart against Stress(Special Lecture 2,Special Program,The 72nd Annual Scientific Meeting of the Japanese Circulation Society)

Vatner Stephen F., Yan Lin, Ishikawa Yoshihiro, Vatner Dorothy E., Sadoshima junichi

Circulation journal : official journal of the Japanese Circulation Society 72 7 - 7 2008.3

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OJ-013 Typpe 5 adenylyl cyclase plays a major role in regulating autonomic responsse to microgravity in the heart(Autonomic nervous system(02)(H),Oral Presentation(Japanese),The 72nd Annual Scientific Meeting of the Japanese Circulation Society)

Yunzhe Bai, Okumura Satoshi, Tsunematsu Takashi, Jiao Qibin, Ono Shinji, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 72 291 - 291 2008.3

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Cardiac myosin light chain kinase - A new player in the regulation of myosin light chain in the heart

Yoshihiro Ishikawa, Reiko Kurotani

CIRCULATION RESEARCH 102 ( 5 ) 516 - 518 2008.3

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DOI： 10.1161/CIRCRESAHA.108.173005

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Therapeutic targets for heart failure: Beyond beta-adrenergic and renin-angiotensin system blockade

Kousaku Iwatsubo, Yoshihiro Ishikawa

Recent Patents on Cardiovascular Drug Discovery 3 ( 1 ) 37 - 44 2008.1

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DOI： 10.2174/157489008783331661

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Caveolin-3 expression and caveolae are required for isoflurane-induced cardiac protection from hypoxia and ischemia/reperfusion injury

Yousuke T. Horikawa, Hemal H. Patel, Yasuo M. Tsutsumi, Michelle M. Jennings, Michael W. Kidd, Yasuko Hagiwara, Yoshihiro Ishikawa, Paul A. Insel, David M. Roth

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY 44 ( 1 ) 123 - 130 2008.1

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DOI： 10.1016/j.yjmcc.2007.10.003

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Liver infarction due to liver abscess

Akio Ashida, Hiroshi Matsukawa, Jyoji Samejima, Keita Fujii, Hiroyuki Adachi, Yoshihiro Ishikawa, Naoto Kato, Masakazu Kawamoto, Jun Fujisawa, Yasushi Rino, Toshio Imada

DIGESTIVE SURGERY 25 ( 4 ) 258 - 259 2008

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DOI： 10.1159/000144654

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Application of the first principles analysis to evaluate cardiac adenylyl cyclase stimulators in vitro

Haruki Eguchi, Reiko Kurotani, Kouji Otsu, Sayaka Suzuki, Yoshihiro Ishikawa

JOURNAL OF PHARMACOLOGICAL SCIENCES 106 97P - 97P 2008

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New molecular targets in treating congestive heart failure; first principle-based drug design

Yoshihiro Ishikawa, Satoshi Okumura, Haruki Eguchi

JOURNAL OF PHARMACOLOGICAL SCIENCES 106 32P - 32P 2008

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The effect of physiological stresses such as aging on cardiac function in sarcalumenin-deficient mice.

Jiao Qibin, Shimura Miei, Akaike Toru, Takeshima Hiroshi, Ishikawa Yoshihiro, Minamisawa Susumu

Proceedings of Annual Meeting of the Physiological Society of Japan 2008 ( 0 ) 185 - 185 2008

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Sarcalumenin (SAR), a Ca2+-binding protein located in the longitudinal sarcoplasmic reticulum (SR), interacts with cardiac SR Ca2+-ATPase (SERCA2a) to modulate its activity and expression. We have demonstrated that SAR deficiency resulted in mild cardiac dysfunction in young mice (JBC 2005). Since it is well known that SERCA2a activity is decreased with aging, we examined the effects of aging on cardiac function in SAR knockout mice (SAR-KO). Cardiac function assessed by in vivo hemodynamic study and the expression levels of SERCA2a protein were progressively decreased in senescent SARKO (n=13) when compared with senescent wild-type (WT) (n=12) or young SARKO (4month old, n=12). LV dp/dtmax (mmHg/s) was 3897 &plusmn; 134, 7091 &plusmn; 657, and 6836 &plusmn; 298 in senescent SARKO, senescent WT, and young SARKO, respectively. The expression levels of SERCA2a protein (% of young WT) were 28 &plusmn; 8, 84 &plusmn; 17, and 44 &plusmn; 17 in senescent SARKO, senescent WT, and young SARKO, respectively. Interestingly, downregulation of SAR preceded downregulation of SERCA in aging cardiac muscles of wild-type mice . These findings indicated that SAR plays a critical role in age-dependent reduction in cardiac function and SR Ca2+ reuptake. [J Physiol Sci. 2008;58 Suppl:S185]

DOI： 10.14849/psjproc.2008.0_185_4

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The effect of physiological stresses such as aging on cardiac function in sarcalumenin-deficient mice

JIAO Qibin, SHIMURA Miei, AKAIKE Toru, TAKESHIMA Hiroshi, ISHIKAWA Yoshihiro, MINAMISAWA Susumu

Journal of Physiological Sciences 58 ( Supplement ) 2008

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Blockade of T-type calcium channels attenuates smooth muscle cell migration, neointimal formation, and oxygen-induced vascular contraction in rat ductus arteriosus

AKAIKE Toru, YOKOYAMA Utako, JIN Mei Hua, JIAO Qibin, IWAMOTO Mari, ISHIKAWA Yoshihiro, ISHIKAWA Yoshihiro, MINAMISAWA Susumu, MINAMISAWA Susumu

日本小児循環器学会雑誌 24 ( 3 ) 2008

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Growth hormone increases migration of smooth muscle cells in rat ductus arteriosus

Jin Meihua, Akaike Toru, Quan Hong, Jiao Qibin, Iwasaki Shiho, Ishikawa Yoshihiro, Minamisawa Susumu

Proceedings of Annual Meeting of the Physiological Society of Japan 2008 ( 0 ) 189 - 189 2008

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The ductus arteriosus (DA), a fetal arterial connection between the pulmonary artery and the descending aorta, is essential for fetal circulation. After birth, the DA closes immediately through the contraction of its smooth muscle. In addition, intimal cushion formation (ICF) plays an important role in DA closure. Since a number of studies have indicated an important role of growth hormone (GH) and insulin-like growth factor (IGF) on cardiovascular development and tissue growth response, we hypothesized that growth hormone may play a role in ICF of DA. We found that the expression of GH receptor (GHR) mRNA in DA was eight times higher than that in aorta, and the GHR was up-regulated in DA during a perinatal period. Immunohistochemical analysis revealed that GHR was predominantly expressed in the endothelium and smooth muscle layer of DA. Using modified Boyden chamber method, the migration of DA smooth muscle cells (SMC) was significantly promoted by 50% in the presence of 20ng/mg GH in the condition media. We found that GH has no effect on SMC proliferation and hyaluronic acid production. These results suggested that GH play a role in intimal cushion formation though increasing migration of DA SMCs. [J Physiol Sci. 2008;58 Suppl:S189]

DOI： 10.14849/psjproc.2008.0_189_2

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A role of rising oxygen tension on smooth muscle cell migration in the rat ductus arteriosus

Akaike Toru, Yokoyama Utako, Jiao Qibin, Jin Mei Hua, Quan Hong, Ishikawa Yoshihiro, Minamisawa Susumu

Proceedings of Annual Meeting of the Physiological Society of Japan 2008 ( 0 ) 189 - 189 2008

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Objective Intimal cushion formation (ICF) is a characteristic vascular remodeling process in the ductus arteriosus (DA). Progressive smooth muscle cell (SMC) migration results in ICF immediately after birth in rodents. We hypothesized that rising oxygen tension plays a role in SMC migration after birth. Methods and Results 1) Isolated SMCs from rat termed-fetal DA were cultured in a hypoxic condition (1% oxygen; the hypoxic group). To investigate the effect of rising oxygen tension on SMC migration, they were transferred in a normoxic condition (21% oxygen; the normoxic group). Using a modified Boyden chamber method, we found that SMC migration was increased by 2.1-fold in the normoxic group when compared with that in the hypoxic group (p<0.05). 2) Since our previous DNA microarray analysis has identified several gene candidates that respond to changes from fetal to neonatal circulation and play a role in migration and proliferation, we examined the direct effect of oxygen on the expression of these genes. Rising oxygen tension from 1% to 21% significantly up-regulated the expression of early growth response gene-1 (3.0-fold), endothelin-1 (2.7-fold), cyclooxygenase-2 (1.9-fold), and fibronectin (1.9-fold) mRNAs in cultured rat DA SMCs. Conclusion Rising oxygen tension promotes migration and regulates gene transcription in rat DA SMCs. These findings may contribute to profound ICF after birth. [J Physiol Sci. 2008;58 Suppl:S189]

DOI： 10.14849/psjproc.2008.0_189_4

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Dopamine induces apoptosis in young, but not in neonatal, neurons via Ca2+-dependent signal

Kousaku Iwatsubo, Sayaka Suzuki, Chanxia Li, Takashi Tsunematsu, Fumi Nakamura, Satoshi Okumura, Motohiko Sato, Susumu Minamisawa, Yoshiyuki Toya, Satoshi Umemura, Yoshihiro Ishikawa

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY 293 ( 5 ) C1498 - C1508 2007.11

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DOI： 10.1152/ajpcell.00088.2007

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Cardiac Overexpression of Epac1 in Transgenic Mice Protects Heart form Lipopolysaccharide-induced Cardiac Dysfunction and Inhibits JAK-STAT Pathway.

Satoshi Okumura, Yunzhe Bai, Meihua Jin, Sayaka Suzuki, Akiko Kuwae, Reiko Kurotani, Yoshihiro Ishikawa

CIRCULATION 116 ( 16 ) 246 - 246 2007.10

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Blockade of T-type calcium channels attenuates smooth muscle cell migration, neointimal formation, and oxygen-induced vascular contraction in rat ductus arteriosus

Toru Akaike, Utake Yokoyama, Jiao Qibin, Mei H. Jin, Hong Quan, Mari Iwamoto, Yoshihiro Ishikawa, Susumu Minamisawa

CIRCULATION 116 ( 16 ) 152 - 152 2007.10

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Isoform-selective regulation of adenylyl cyclase by forskolin derivatives: prediction of selectivity by computer-based analysis

Haruki Eguchi, Kousaku Iwatsubo, Yoshihiro Ishikawa

LETTERS IN DRUG DESIGN & DISCOVERY 4 ( 6 ) 434 - 441 2007.9

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DOI： 10.2174/157018007781387755

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ラット動脈管におけるT型カルシウムチャンネルの役割の検討

赤池徹, 横山詩子, 岩本眞理, 石川義弘, 南沢享

脈管学 47 ( Suppl. ) S227 - S227 2007.9

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Developmental changes in gene expression of Epac and its upregulation in myocardial hypertrophy

Coskun Ulucan, Xu Wang, Erdene Baljinnyam, Yunzhe Bai, Satoshi Okumura, Motohiko Sato, Susumu Minamisawa, Shinichi Hirotani, Yoshihiro Ishikawa

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY 293 ( 3 ) H1662 - H1672 2007.9

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DOI： 10.1152/ajpheart.00159.2007

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Type 5 adenylyl cyclase disruption increases longevity and protects against stress

Lin Yan, Dorothy E. Vatner, J. Patrick O'Connor, Andreas Ivessa, Hui Ge, Wei Chen, Shinichi Hirotani, Yoshihiro Ishikawa, Junichi Sadoshima, Stephen F. Vatner

CELL 130 ( 2 ) 247 - 258 2007.7

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DOI： 10.1016/j.cell.2007.05.038

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cAMP依存性動脈管内膜肥厚の分子機序

南沢享, 赤池徹, 横山詩子, 石川義弘

循環制御 28 ( Suppl. ) 56 - 56 2007.5

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Catecholamine-induced apoptosis in striatal neurons from 2 weeks old mice using a newly developed culture technique

Sayaka Suzuki, Kousaku Iwatsubo, Takashi Tsunematsu, Fumi Nakamura, Otsu Koji, Yoshihiro Ishikawa

FASEB JOURNAL 21 ( 6 ) A1342 - A1342 2007.4

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Caveolin improves glucose metabolism in diabetic mice

Koji Otsu, Yoshiyuki Toya, Jin Oshikawa, Masahiro Sakata, Takuya Yazawa, Satoshi Okumura, Motohiko Sato, Satoshi Umemura, Susumu Minamisawa, Yoshihiro Ishikawa

FASEB JOURNAL 21 ( 6 ) A833 - A833 2007.4

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Developmental changes in Epac gene expression in mice

Coskun Ulucan, Xu Wang, Erdenechimeg Baljinnyam, Yoshihiro Ishikawa

FASEB JOURNAL 21 ( 6 ) A1152 - A1152 2007.4

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OE-321 Identification of a Novel G-protein Activator Induced by Cardiac Ischemia/hypoxia(Molecular biology, myocardium-1, The 71st Annual Scientific Meeting of the Japanese Circulation Society)

Sato Motohiko, Lanier Stephen M, Toyota Eiji, Cismowski Mary J, Smrcka Alan V, Chilian William M, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 71 231 - 231 2007.3

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FRS-081 T-type Calcium Channels Regulate Oxygen-induced Vascular Contraction and Smooth Muscle Cell Migration in the Rat Ductus Arteriosus(Molecular Biology in Cardiovascular Diseases (basic), The 71st Annual Scientific Meeting of the Japanese Circulation Society)

Akaike Toru, Yokoyama Utako, Quan Hong, Iwamoto Mari, Ishikawa Yoshihiro, Minamisawa Susumu

Circulation journal : official journal of the Japanese Circulation Society 71 139 - 139 2007.3

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OE-158 Epac1 Promotes Intimal Cushion Formation of the Rat Ductus Arteriosus by Enhancing Smooth Muscle Cell Migration(Congenital heart disease/Kawasaki's disease-1, The 71st Annual Scientific Meeting of the Japanese Circulation Society)

Akaike Toru, Yokoyama Utako, Quan Hong, Iwamoto Mari, Ishikawa Yoshihiro, Minamisawa Susumu

Circulation journal : official journal of the Japanese Circulation Society 71 190 - 190 2007.3

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5 Vascular Injury-induced Upregulation of Epac1 Counteracts PKA, Promoting Smooth Muscle Cell Migration and Neointimal Thickening(The 71st Annual Scientific Meeting of the Japanese Circulation Society)

Yokoyama Utako, Minamisawa Susumu, Ulucan Coskun, Wang Xu, Baljinnyam Erdenechimeg, Takaoka Minoru, Hong Quan, Otsu Koji, Sata Masataka, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 71 52 - 52 2007.3

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Altered autonomic control in conscious transgenic rabbits with overexpressed cardiac Gs alpha

Takao Nishizawa, You-Tang Shen, Franco Rossi, Chull Hong, Jeffrey Robbins, Yoshihiro Ishikawa, Junichi Sadoshima, Dorothy E. Vatner, Stephen F. Vatner

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY 292 ( 2 ) H971 - H975 2007.2

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DOI： 10.1152/ajpheart.00791.2006

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ラット動脈管の内膜クッション形成のEpac1による促進(Epac 1 promotes intimal cushion formation of the rat ductus arteriosus)

赤池徹, 南沢享, 横山詩子, 全紅, 岩本眞理, 横田俊平, 石川義弘

日本小児科学会雑誌 111 ( 2 ) 302 - 302 2007.2

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ラット動脈管の血管収縮と平滑筋細胞の遊走におけるT型Ca2+channelの機能の検討

赤池徹, 南沢享, 横山詩子, 全紅, 岩本眞理, 横田俊平, 石川義弘

日本小児科学会雑誌 111 ( 2 ) 302 - 302 2007.2

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T-type calcium channels (TCC) control oxygen-induced vascular contraction and remodeling in the rat ductus arteriousus (DA).

AKAIKE Toru, YOKOYAMA Utako, QUAN Hong, WATANABE Mayumi, IWAMOTO Mari, YOKOTA Syumpei, ISHIKAWA Yoshihiro, MINAMISAWA Susumu

Pediatrics International 49 ( 5 ) 2007

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Epac1はラット動脈管の内膜肥厚形成を促進する(原標題は英語)

赤池徹, 南沢享, 横山詩子, 全紅, 岩本眞理, 横田俊平, 石川義弘

日本小児科学会雑誌 111 ( 2 ) 2007

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T-type calcium channels regulate oxygen-induced vascular contraction and smooth muscle cell migration in the rat DA

Akaike Toru, Yokoyama Utako, Quan Hong, Ishikawa Yoshihiro, Minamisawa Susumu

Proceedings of Annual Meeting of the Physiological Society of Japan 2007 ( 0 ) 80 - 80 2007

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Objective Ca2+ influx through voltage-dependent Ca2+ channels regulates vascular contraction and remodeling. However, the role of T-type Ca2+ channels (TCCs) has remained unknown in the ductus arteriosus (DA). Methods and Results 1) &alpha;1G, a major isoform of TCC in DA, was significantly up-regulated after birth. &alpha;1G was localized in the region of intimal thickening in rat perinatal DA. When the condition of culture media was changed from hypoxia (1% oxygen) to normoxia (21% oxygen), the expression of &alpha;1G mRNA was up-regulated by 1.5 fold in DA smooth muscle cells (SMCs), suggesting that the increase in oxygen tension is associated with the up-regulation of &alpha;1G mRNA in rat DA. 2) A highly selective TCC blocker, R(-)-efonidipine, significantly attenuated oxygen-induced vasoconstriction by 74% in rat DA at embryonic day 21 (p<0.01). The combination of a L-type Ca2+ channel blocker, nitrendipine, and R(-)-efonidipine induced further relaxation of DA, suggesting the additive effect of LCC and TCC. 3) DA SMC migration was increased in an extracellular Ca2+ concentration-dependent manner. DA SMC migration and proliferation were significantly decreased by stimulation of R(-)-efonidipine and by inhibition of &alpha;1G expression using &alpha;1G-specific siRNA. These data suggested that TCC promotes SMC migration and proliferation in rat DA. Conclusion TCC, which was up-regulated upon exposure to oxygen, regulated postnatal oxygen-induced DA closure through vasoconstriction and SMC migration and proliferation. [J Physiol Sci. 2007;57 Suppl:S80]

DOI： 10.14849/psjproc.2007.0_080_2

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T-type calcium channels regulate oxygen-induced vascular contraction and smooth muscle cell migration in the rat DA

AKAIKE Toru, YOKOYAMA Utako, QUAN Hong, ISHIKAWA Yoshihiro, MINAMISAWA Susumu

Journal of Physiological Sciences 57 ( Supplement ) 2007

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T-type Calcium Channels Regulate Oxygen-induced Vascular Contraction and Smooth Muscle Cell Migration in the Rat Ductus Arteriosus

AKAIKE Toru, YOKOYAMA Utako, QUAN Hong, IWAMOTO Mari, ISHIKAWA Yoshihiro, MINAMISAWA Susumu

Circulation Journal 71 ( Supplement 1 ) 2007

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Epac1 Promotes Intimal Cushion Formation of the Rat Ductus Arteriosus by Enhancing Smooth Muscle Cell Migration

AKAIKE Toru, YOKOYAMA Utako, QUAN Hong, IWAMOTO Mari, ISHIKAWA Yoshihiro, MINAMISAWA Susumu

Circulation Journal 71 ( Supplement 1 ) 2007

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The gene transfer of caveolin improves glucose metabolism in diabetic mice.

Jin Oshikawa, Yoshiyuki Toya, Koji Otsu, Toshiharu Kokuho, Tatsuo Hashimoto, Tadashi Kuji, Koichi Tamura, Satoshi Umemura, Yoshihiro Ishikawa

JOURNAL OF HYPERTENSION 24 386 - 386 2006.12

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Role of the calcium modulated cyclases in the development of the retinal projections

Xavier Nicol, Mohammed Bennis, Yoshihiro Ishikawa, Guy C. -K. Chan, Jacques Reperant, Daniel R. Storm, Patricia Gaspar

EUROPEAN JOURNAL OF NEUROSCIENCE 24 ( 12 ) 3401 - 3414 2006.12

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DOI： 10.1111/j.1460-9568.2006.05227.x

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Chronic activation of the prostaglandin recepor EP4 promotes hyaluronan-mediated neointimal formation in the ductus arteriosus

Utako Yokoyama, Susumu Minamisawa, Hong Quan, Shibnath Ghatak, Toru Akaike, Eri Segi-Nishida, Shiho Iwasai, Mari Iwamoto, Suniti Misra, Kouichi Tamura, Hideaki Hori, Shumpei Yokota, Bryan P. Toole, Yukihiko Sugimoto, Yoshihiro Ishikawa

JOURNAL OF CLINICAL INVESTIGATION 116 ( 11 ) 3026 - 3034 2006.11

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DOI： 10.1172/JCI28639

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Drug therapy aimed at adenylyl cyclase to regulate cyclic nucleotide signaling

Kousaku Iwatsubo, Satoshi Okumura, Yoshihiro Ishikawa

Endocrine, Metabolic and Immune Disorders - Drug Targets 6 ( 3 ) 239 - 247 2006.9

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DOI： 10.2174/187153006778249994

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Overexpressed cardiac Gs alpha in rabbits

Takao Nishizawa, Stephen F. Vatner, Chull Hong, You-Tang Shen, Stefan E. Hardt, Jeffrey Robbins, Yoshihiro Ishikawa, Junichi Sadoshima, Dorothy E. Vatner

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY 41 ( 1 ) 44 - 50 2006.7

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DOI： 10.1016/j.yjmcc.2006.03.008

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Post-transcriptional downregulation of sarcolipin mRNA by triiodothyronine in the atrial myocardium

S Minamisawa, N Uemura, Y Sato, U Yokoyama, T Yamaguchi, K Inoue, M Nakagome, YZ Bai, H Hori, M Shimizu, S Mochizuki, Y Ishikawa

FEBS LETTERS 580 ( 9 ) 2247 - 2252 2006.4

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DOI： 10.1016/j.febslet.2006.03.032

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OJ-202 The Prostaglandin E Specific-receptor EP4 Plays an Essential Role in Hyaluronan-induced Neointimal Formation in Ductus Arteriosus(Congenital heart disease/Kawasaki's disease-1 (M) OJ34,Oral Presentation (Japanese),The 70th Anniversary Annual Scientific Meeting of the Japanese Circulation Society)

Yokoyama Utako, Minamisawa Susumu, Segi-Nishida Eri, Tamura Koichi, Iwamoto Mari, Yokota Shumpei, Sugimoto Yukihiko, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 70 284 - 284 2006.3

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OJ-022 Sarcalumenin Plays a Critical Role in SERCA2a Stability and Adaptation to Sustained Biomechanical Stresses in the Failing Heart(Heart failure, basic-2 (M) OJ4,Oral Presentation (Japanese),The 70th Anniversary Annual Scientific Meeting of the Japanese Circulation Society)

Shimura Miei, Minamisawa Susumu, Takeshima Hiroshi, Ishikawa Toshiyuki, Uchino Kazuaki, Kimura Kazuo, Ishikawa Yoshihiro, Umemura Satoshi

Circulation journal : official journal of the Japanese Circulation Society 70 239 - 239 2006.3

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PE-551 Adenylyl Cyclase Type 2 and 5/6 Differently Regulate Vascular Tone and Remodeling in the Rat Ductus Arteriosus(Congenital heart disease/Kawasaki's disease-2 (M) PE94,Poster Session (English),The 70th Anniversary Annual Scientific Meeting of the Japanese Circulation Society)

Minamisawa Susumu, Yokoyama Utako, Tsunematsu Takashi, Iwatsubo Kosaku, Yokota Shumpei, Iwamoto Mari, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 70 470 - 470 2006.3

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Caveolin regulates microtubule polymerization in the vascular smooth muscle cells

J Kawabe, S Okumura, MA Nathanson, N Hasebe, Y Ishikawa

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 342 ( 1 ) 164 - 169 2006.3

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DOI： 10.1016/j.bbrc.2006.01.125

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ビタミンAがラット動脈管遺伝子発現プロファイルに及ぼす影響

南沢享, 横山詩子, 石川義弘, 岩本眞理, 横田俊平, 佐藤陽治

日本小児循環器学会雑誌 22 ( 2 ) 108 - 109 2006.3

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動脈管におけるPGE1のヒアルロン酸産生効果

横山詩子, 南沢享, 石川義弘, 岩本眞理, 横田俊平

日本小児循環器学会雑誌 22 ( 2 ) 109 - 109 2006.3

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ラット動脈管における2型,5/6型アデニル酸シクラーゼの選択的血管拡張作用と血管リモデリング効果

横山詩子, 南沢享, 常松尚志, 岩坪耕策, 堀英明, 横田俊平, 石川義弘

血管 29 ( 1 ) 26 - 26 2006.1

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Application of the first principle analysis to evaluate cardiac adenylyl cyclase stimulators

H Eguchi, K Iwatsubo, Y Ishikawa

JOURNAL OF PHARMACOLOGICAL SCIENCES 100 86P - 86P 2006

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Genetic manipulation and functional analysis of cAMP signalling in cardiac muscle: implications for a new target of pharmacotherapy

Y Ishikawa, K Iwatsubo, T Tsunematsu, S Okumura

BIOCHEMICAL SOCIETY TRANSACTIONS 33 1337 - 1340 2005.12

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DOI： 10.1042/BST20051337

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Caveolin; different roles for insulin signal?

Y Ishikawa, K Otsu, J Oshikawa

CELLULAR SIGNALLING 17 ( 10 ) 1175 - 1182 2005.10

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DOI： 10.1016/j.cellsig.2005.03.025

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Disruption of type 5 adenylyl cyclase enhances desensitization of the camp signal and increases the Akt signal following chronic catecholamine stress, protecting myocyte viability

S Okumura, J Liu, GP Yang, C Ulucan, T Tsunematsu, J Kawabe, Y Ishikawa

CIRCULATION 112 ( 17 ) U313 - U313 2005.10

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Prostaglandin EP4 signal promotes the vascular remodeling and closure of the rat ductus arteriosus

U Yokoyama, S Minamisawa, S Yokota, Y Ishikawa

CIRCULATION 112 ( 17 ) U92 - U92 2005.10

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Disruption of sarcalumenin accelerated pressure overload-induced heart failure in mice

M Shimura, S Minamisawa, H Takeshima, S Umemura, Y Ishikawa

CIRCULATION 112 ( 17 ) U67 - U67 2005.10

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インスリンシグナル増強因子3型(筋型)カベオリンの遺伝子導入は高脂肪食マウスのインスリン抵抗性を改善する

戸谷義幸, 大津恒治, 押川仁, 岩坪耕策, 田村功一, 平和伸仁, 木原実, 石上友章, 萩原康子, 南沢享, 梅村敏, 石川義弘

日本高血圧学会総会プログラム・抄録集 28回 35 - 35 2005.9

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心不全進展のメカニズムを考慮した分子レベルからの新たな心不全治療戦略成人期の心臓に特異的発現を示す5型アデニル酸シクラーゼの心不全発症に果たす役割とその特異的抑制薬による新しい心不全治療

奥村敏, 稲見茂信, 高野雅充, 大場崇芳, 水野杏一, 高野照夫, 常松尚志, 石川義弘

Journal of Cardiology 46 ( Suppl.I ) 140 - 140 2005.8

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Sarcalumenin Deficiency Induced Cardiac Dysfunction in Mice(Excitation-contraction Coupling/Ion Channel 1 (A), The 69th Annual Scientific Meeting of the Japanese Circulation Society)

Shimura Miei, Minamisawa Susumu, Ishikawa Toshiyuki, Uchino Kazuaki, Saeki Yasutake, Kimura Kazuo, Ishikawa Yoshihiro, Umemura Satoshi

Circulation journal : official journal of the Japanese Circulation Society 69 193 - 193 2005.3

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A Novel Alternatively Spliced Variant of the Voltage-dependent Calcium Channel α 1C Isoform in the Rat Vascular and Airway Smooth Muscles (Vascular Smooth Muscle 2 (H), The 69th Annual Scientific Meeting of the Japanese Circulation Society)

Minamisawa Susumu, Yokoyama Utako, Yokota Shumpei, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 69 556 - 556 2005.3

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Adenylyl Cyclase Type II Stimulation Inhibited Indomethacin-induced Contraction of Vascular Smooth Muscle in the Rat Ductus Arteriosus(Congenital Heart Disease/Kawasaki's Disease 3 (M), The 69th Annual Scientific Meeting of the Japanese Circulation Society)

Yokoyama Utako, Minamisawa Susumu, Tsunematsu Takashi, Iwatsubo Kosaku, Iyokota shumpei, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 69 419 - 419 2005.3

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Type 5 Adenylyl Cyclase is Preferentially Coupled to β1-adrenoceptor Subtype in Cardiomyocytes(Cardiac Function, Basic/Clinical 3 (M), The 69th Annual Scientific Meeting of the Japanese Circulation Society)

Tsunematsu Takashi, Okumura Satoshi, Iwatsubo Kosaku, Minamisawa Susumu, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 69 234 - 234 2005.3

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Effects of Chronic Beta-Adrenergic Receptor Stimulation in Type 5 Adenylyl Cyclase-Null Mice(Heart Failure, Basic 1 (M), The 69th Annual Scientific Meeting of the Japanese Circulation Society)

Okumura Satoshi, Tomita Kazunori, Murakami Daisuke, Ogawa Beni, Tajika Kenichiro, Tokuyama Kenichi, Inami Shigenobu, Takano Masamichi, Seimiya Koji, Ohba Takayoshi, Kawaguchi Naomi, Nomura Atsunobu, Mizuno Kyoichi, Takano Teruo, Tsunematsu Takashi, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 69 157 - 157 2005.3

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Congenital semilunar valvulogenesis defect in mice deficient in phospholipase C epsilon

M Tadano, H Edamatsu, S Minamisawa, U Yokoyama, Y Ishikawa, N Suzuki, H Saito, DM Wu, M Masago-Toda, Y Yamawaki-Kataoka, T Setsu, T Terashima, S Maeda, T Satoh, T Kataoka

MOLECULAR AND CELLULAR BIOLOGY 25 ( 6 ) 2191 - 2199 2005.3

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DOI： 10.1128/MCB.25.6.2191-2199.2005

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The relaxing effects of adenylyl cyclase type II stimulator in vascular smooth muscle of rat ductus arteriosus

U Yokoyama, S Minamisawa, T Tsunematsu, K Iwatsubo, Y Ishikawa

FASEB JOURNAL 19 ( 5 ) A1622 - A1622 2005.3

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Transgenic mice overexpressing sarcolipin in the heart exhibited cardiac dysfunction

S Minamisawa, N Uemura, M Shimura, U Yokoyama, Y Ishikawa

FASEB JOURNAL 19 ( 4 ) A560 - A560 2005.3

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Sarcalumenin ablation induced cardiac dysfunction in mice

M Shimura, S Minamisawa, H Takeshima, Y Saeki, Y Ishikawa, S Umemura

FASEB JOURNAL 19 ( 4 ) A559 - A559 2005.3

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Impaired Ca2+ store functions in skeletal and cardiac muscle cells from sarcalumenin-deficient mice

M Yoshida, S Minamisawa, M Shimura, S Komazaki, H Kume, M Zhang, K Matsumura, M Nishi, M Saito, Y Saeki, Y Ishikawa, T Yanagisawa, H Takeshima

JOURNAL OF BIOLOGICAL CHEMISTRY 280 ( 5 ) 3500 - 3506 2005.2

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DOI： 10.1074/jbc.M406618200

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5型アデニル酸シクラーゼ特異的抑制薬を用いた心筋細胞アポトーシス阻止

岩坪耕策, 南沢享, 常松尚志, 戸谷義幸, 梅村敏, 石川義弘

血管 28 ( 1 ) 2 - 2 2005.1

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Junctophilin type 2 is associated with caveolin-3 and is down-regulated in the hypertrophic and dilated cardiomyopathies

S Minamisawa, J Oshikawa, H Takeshima, M Hoshijima, YB Wang, KR Chien, Y Ishikawa, R Matsuoka

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 325 ( 3 ) 852 - 856 2004.12

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DOI： 10.1016/j.bbrc.2004.10.107

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Down-regulation of sarcolipin mRNA expression in chronic atrial fibrillation

N Uemura, T Ohkusa, K Hamano, M Nakagome, H Hori, M Shimizu, M Matsuzaki, S Mochizuki, S Minamisawa, Y Ishikawa

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION 34 ( 11 ) 723 - 730 2004.11

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DOI： 10.1111/j.1365-2362.2004.01422.x

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Adverse effects of chronic pressure overload in mice with type 5 adenylyl cyclase overexpression and its reversal by beta-adrenergic blockade

J Liu, Y Ishikawa, J Thaisz, DE Vatner, SF Vatner

CIRCULATION 110 ( 17 ) 66 - 66 2004.10

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Genetic ablation of phospholipase C-epsilon resulted in defective cardiac semilunar valve formation

S Minamisawa, M Tadano, H Edamatsu, U Yokoyama, Y Ishikawa, N Suzuki, H Saito, T Satoh, T Kataoka

CIRCULATION 110 ( 17 ) 93 - 93 2004.10

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Effects of Colforsin Daropate Hydrochloride(Adehl^【○!R】 Inj.), Anti-Acute Heart Failure Agent, on Adenylate Cyclase-Related Hormone Actions

TAMAKI Satoru, HOSODA Saichi, ISHIKAWA Yoshihiro, FUJIHARA Ryo, HASUNUMA Tomoko, NAKAMURA Masahiko, IWASAWA Kuniaki, YAMASHITA Hiroshi, MATSUDA Hiroyuki, KUROSU Tetsuya, UEBABA Kazuo, KOMIYAMA Kanki

Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 35 ( 5 ) 235 - 246 2004.9

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DOI： 10.3999/jscpt.35.5_235

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ニコチン受容体の細胞膜局在性--ラフトを介したニコチン受容体とアデニル酸シクラーゼの共役 (ニコチン受容体サブタイプと生体機能--新しい創薬ターゲット)

押川仁, 石川義弘

医学のあゆみ 210 ( 7 ) 669 - 671 2004.8

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Other Link： http://search.jamas.or.jp/link/ui/2005050889
Insulin resistance in skeletal muscles of caveolin-3-null mice

J Oshikawa, K Otsu, Y Toya, T Tsunematsu, R Hankins, J Kawabe, S Minamisawa, S Umemura, Y Hagiwara, Y Ishikawa

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 101 ( 34 ) 12670 - 12675 2004.8

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DOI： 10.1073/pnas.0402053101

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Translocation of caveolin regulates stretch-induced ERK activity in vascular smooth muscle

J Kawabe, S Okumura, MC Lee, J Sadoshima, Y Ishikawa

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY 286 ( 5 ) H1845 - H1852 2004.5

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DOI： 10.1152/ajpheart.00593.2003

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PLCepsilonはマウス正常大動脈弁形成に必須である

南沢享, 多々野誠, 枝松裕紀, 横山詩子, 石川義弘, 片岡徹

日本小児循環器学会雑誌 20 ( 3 ) 267 - 267 2004.5

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OJ-513 Caveolin Modulates Microtubule Polymerization in Vascular Smooth Muscle Cells (VSMC)(Vascular Smooth Muscle 2 (H) : OJ63)(Oral Presentation (Japanese))

Kawabe Junichi, Ishikawa Yoshihiro, Hasebe Naoyuki, Kikuchi Kenjiro

Circulation journal : official journal of the Japanese Circulation Society 68 355 - 355 2004.3

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OJ-018 Left-sided Pressure Overload Down-regulated the Expression of Sarcolipin mRNA Preferentially in the Left Atrium(Excitation-Contraction Coupling/Ion Channel (A) : OJ3)(Oral Presentation (Japanese))

Shimura Miei, Minamisawa Susumu, Ishikawa Toshiyuki, Uchino Kazuaki, Kimura Kazuo, Ishikawa Yoshihiro, Umemura Satoshi

Circulation journal : official journal of the Japanese Circulation Society 68 236 - 236 2004.3

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PE-094 β-adrenergic and Muscarinic Regulation of the Heart Requires Type 5 Adenylyl Cyclase(Autonomic Nervous System 1 (H) : PE16)(Poster Session (English))

Okumura Satoshi, Kawabe Junichi, Takagi Gen, Takano Teruo, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 68 385 - 385 2004.3

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OE-109 Disruption of the Type 5 Adenylyl Cyclase Gene Preserves Cardiac Function Against Pressure Overload(Heart Failure, Basic 1 (M) : OE13)(Oral Presentation (English))

Okumura Satoshi, Kawabe Junichi, Takagi Gen, Takano Teruo, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 68 167 - 167 2004.3

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FRS-018 The Type 5 Adenylyl Cyclase Mediates Ca^<2+>-mediated Regulation of Ca^<2+> channels in the Heart(Cardiac Hypertrophy (M) : FRS3)(Featured Research Session (English))

Ishikawa Yoshihiro, Yatani Atsuko, Kawabe Junichi, Takano Teruo, Okumura Satoshi

Circulation journal : official journal of the Japanese Circulation Society 68 94 - 94 2004.3

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OJ-015 Retinoic acid and thyroid hormones play an important role in the transcriptional regulation of sarcolipin(Excitation-Contraction Coupling/Ion Channel (A) : OJ3)(Oral Presentation (Japanese))

Minamisawa Susumu, Satoh Yoji, Uemura Nobuyuki, Yokoyama Utako, Mochizuki Seibu, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 68 235 - 235 2004.3

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OJ-514 Translocation of Caveolin Regulates Stretch-Induced Extracellular Signal-Regulated Kinase (ERK) Activity in Vascular Smooth Muscle Cells (VSMC)(Vascular Smooth Muscle 2 (H) : OJ63)(Oral Presentation (Japanese))

Kawabe Junichi, Ishikawa Yoshihiro, Hasebe Naoyuki, Kikuchi Kenjiro

Circulation journal : official journal of the Japanese Circulation Society 68 355 - 355 2004.3

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Development of insulin resistance in caveolin-3 knockout mice

J Oshikawa, Y Toya, K Otsu, R Hankins, T Tsunematsu, S Minamisawa, S Umemura, Y Hagiwara, Y Ishikawa

FASEB JOURNAL 18 ( 5 ) A1120 - A1120 2004.3

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Preferential coupling of type 5 adenylyl cyclase to beta 1-adrenoceptor subtype in cardiomyocytes

T Tsunematsu, S Okumura, K Iwatsubo, Y Ishikawa

FASEB JOURNAL 18 ( 5 ) A1076 - A1076 2004.3

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Caveolin-3 overexpression stimulates insulin signal in hepatic cells

K Otsu, J Oshikawa, J Kawabe, Y Ishikawa

FASEB JOURNAL 18 ( 4 ) A137 - A137 2004.3

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Oxidized galectin-1 stimulates macrophages to promote axonal regeneration in peripheral nerves after axotomy

H Horie, T Kadoya, N Hikawa, K Sango, H Inoue, K Takeshita, R Asawa, T Hiroi, M Sato, T Yoshioka, Y Ishikawa

JOURNAL OF NEUROSCIENCE 24 ( 8 ) 1873 - 1880 2004.2

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DOI： 10.1523/JNEUROSCI.4483-03.2004

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3型カベオリン遺伝子導入によるインスリン感受性の増強作用

大津恒治, 押川仁, 南沢享, 堀英明, 石川義弘

日本生理学雑誌 66 ( 1 ) 38 - 38 2004.1

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Characterization of adenylyl cyclase isoforms in the rat ductus arteriosus

Mouri Maya, Yokoyama Utako, Tsunematsu Takashi, Iwatubo Kousaku, Hori Hideaki, Minamisawa Susumu, Ishikawa Yosihiro

Proceedings of Annual Meeting of the Physiological Society of Japan 2004 ( 0 ) S94 - S94 2004

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The ductus arteriosus (DA), a fetal connection between the pulmonary artery and the aorta, plays an important role in in utero cardiovascular circulation. Prostaglandin E (PGE) plays a principal role in maintaining the patency of the DA. The DA displays the higher sensitivity to PGE than other vascular smooth muscles. PGE activates adenylyl cyclases (ACs) via the EP4 receptor, resulting in an increase in the intracellular cAMP in the DA. ACs consist of 9 isoforms that demonstrate distinct tissue distribution and function. However, characterization of ACs remain undetermined in the DA. We examined the expression of AC isoform mRNAs in the DA by semi-quantitative and quantitative RT-PCR. Pooled tissues of the DA were obtained from Wistar rat embryos at embryonic day19 and day21, and neonates on the day of birth. AC2, AC3, AC4, AC5, AC6, AC7, and AC9 were expressed in the DA, while AC1 and AC8 were not detected. The expression of AC2, AC4, and AC6 mRNAs in the DA were significantly higher than that in the aorta. In particular, AC2 was expressed to a strikingly higher degree in the DA at embryonic day21 and the day of birth (~ 30% increase) than in the adult aorta. The expression of AC3, AC5, and AC7 mRNAs in the DA were comparable with those in the aorta. The present study identified multiple AC isoforms in the rat DA. AC2, AC4 and AC6 isoforms, in particular AC2, may play an important role in mediating PGE signal in the DA. [Jpn J Physiol 54 Suppl:S94 (2004)]

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Interleukin-12 p40-homodimer production in sensory dorsal root ganglion neurons

N Hikawa, Y Ishikawa, T Takenaka

NEUROSCIENCE 129 ( 1 ) 75 - 83 2004

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DOI： 10.1016/j.neuroscience.2004.07.035

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Down-regulation of the sarcolipin mRNA expression in the atrium of patients with chronic atrial fibrillation

N Uemura, T Ohkusa, S Minamisawa, K Hamano, S Mochizuki, Y Ishikawa

CIRCULATION 108 ( 17 ) 150 - 150 2003.10

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Effects of chronic beta-adrenergic receptor stimulation in type 5 adenylyl cyclase-null mice

S Okumura, J Kawabe, GP Yang, L Jing, J Sadoshima, SF Vatner, Y Ishikawa

CIRCULATION 108 ( 17 ) 48 - 48 2003.10

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Pharmacological Inhibition of Cardiac Adenylyl Cyclase in an Isoform-Specific Manner

Iwatsubo Kousaku, Minamisawa Susumu, Toya Yoshiyuki, Tsunematsu Takashi, Iwamoto Tamio, Umemura Satoshi, Ishikawa Yoshihiro

Circulation journal : official journal of the Japanese Circulation Society 67 170 - 171 2003.3

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Sarcolipin, a Novel Calcium Regulator, Is Preferentially Expressedin the Atrium and Is Downregulated in the Hypertrophic Heart

Minamisawa Susumu, Uemura Nobuyuki, Ishikawa Yoshihiro, Wang Yibin, Chen Ju, Chien Kenneth R., Matsuoka Rumiko

Circulation journal : official journal of the Japanese Circulation Society 67 211 - 211 2003.3

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Coordinated motor dysfunction in type 5 adenylyl-cyclase deficient mice

T Iwamoto, S Okumura, K Iwatsubo, J Kawabe, Y Toya, S Umemura, N Arai, Y Goshima, CJ Homcy, SF Vatner, Y Ishikawa

FASEB JOURNAL 17 ( 4 ) A204 - A204 2003.3

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Adenylyl cyclase type 5 disruption preserves cardiac function in response to pressure overload

G Takagi, S Okumara, J Kawabe, C Hong, GP Yang, T Meguro, Takagi, I, A Yatani, Gaussin, V, DE Vatner, J Sadoshima, CJ Homcy, Y Ishikawa, SF Vatner

CIRCULATION 106 ( 19 ) 59 - 59 2002.11

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Pharmacological inhibition of cardiac adenylyl cyclase in an isoform-specific manner

K Iwatsubo, S Minamisawa, Y Toya, RM Scarborough, DB Cherbavaz, M Bao, JE Tomlinson, DM Sedlock, DE Levy, S Umemura, CJ Homcy, Y Ishikawa

CIRCULATION 106 ( 19 ) 49 - 49 2002.11

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Blunted autonomic regulation in the hearts of type 5 adenylyl cyclase null mice

S Okumura, G Takagi, J Kawabe, L Lee, C Hong, R Honda, Takagi, I, J Sadoshima, A Yatani, DE Vatner, CJ Homcy, SF Vatner, Y Ishikawa

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY 29 ( 8 ) A78 - A78 2002.8

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Ischemic preconditioning prevents beta(1) adrenergic receptor sequestration

K Iwatsubo, T Fujita, Y Toya, T Onda, T Iwamoto, Sakai, I, Y Hashimoto, Y Ishikawa, S Umemura

JOURNAL OF HYPERTENSION 20 S364 - S364 2002.6

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Calcium plays a major role in caveolin-mediated inhibition of growth signal in the heart

Fujita Takayuki, Hashimoto Yoko, Sakai Ikuko, Ishikawa Yoshihiro, Iwatsubo Kousaku, Toya Yoshiyuki, Umemura Satoshi, Ito Takaaki, Egawa Masato

Circulation journal : official journal of the Japanese Circulation Society 66 672 - 672 2002.3

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Loss of muscarinic regulation in the heart of type V adenylyl cyclase knockout mice

S Okumura, J Kawabe, G Takagi, L Lee, C Hong, Takagi, I, A Yatani, DE Vatner, CJ Homcy, SF Vatner, Y Ishikawa

FASEB JOURNAL 16 ( 5 ) A821 - A821 2002.3

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Translocation of caveolin regulates stretch-mediated extracellular signal-regulated kinase (ERK) activity in vascular smooth muscle cells

J Kawabe, S Okumura, LMC Lee, Y Ishikawa

FASEB JOURNAL 16 ( 4 ) A98 - A98 2002.3

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Caveolin 3 inhibits growth signal in cardiac myoblasts in a calcium-dependent manner

T Fujita, Y Hashimoto, K Iwatsubo, Sakai, I, Y Toya, M Egawa, S Umemura, S Okumura, Y Ishikawa

CIRCULATION 104 ( 17 ) 196 - 197 2001.10

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NKH477, a new inotropic reagent that directly stimulates adenylyl cyclase, does not cause the beta-adrenergic receptor downregulation; Demonstration using a newly developed whole cell binding assays

K Iwatsubo, Y Tao, T Onda, Y Toya, T Fujita, S Umemura, Y Ishikawa

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 37 ( 2 ) 272A - 272A 2001.2

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Accumulation of molecules involved in alpha(1)-adrenergic signal within caveolae; the role of caveolin in the development of cardiac hypertrophy

T Fujita, Y Toya, K Iwatsubo, T Onda, S Umemura, Y Ishikawa

CIRCULATION 102 ( 18 ) 198 - 198 2000.10

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Sema3AはNeuropilin-1とLavendustin A感受性Tyrosine Kinaseを介して後根神経節軸索輸送を促進する

李蝉夏, 堀英明, 佐々木幸生, 川上倫, 石川義弘, 五嶋良郎

日本神経科学大会プログラム・抄録集 23rd 2000

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Molecular variants of human angiotensinogen gene and essential hypertension: A role of a new mutation at intron 1

T Ishigami, T Fujita, K Tamura, K Hibi, M Fukuoka, Nakazawa, I, S Kobayashi, Kobayashi, I, M Kihara, Y Toya, Y Ishikawa, H Ochiai, S Umemura

HYPERTENSION 33 ( 5 ) 1289 - 1289 1999.5

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Molecular variants of human angiotensinogen gene and essential hypertension. A role of a new mutation at intron I

T Ishigami, T Fujita, K Tamura, K Hibi, M Fukuoka, Nakazawa, I, S Kobayashi, Kobayashi, I, M Kihara, Y Toya, Y Ishikawa, H Ochiai, S Umemura

HYPERTENSION 33 ( 4 ) 1080 - 1080 1999.4

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SI-8 心筋の適応と破綻における自律神経の役割

石川義弘, 聴永健, 落合久夫, ステファンバトナー, 梅村敏

Japanese circulation journal 63 ( 1 ) 37 - 37 1999.3

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Inhibition of adenylyl cyclase by caveolin peptides

Y Toya, Y Ishikawa, T Ebina, M Kihara, S Umemura, K Tamura, T Ishigami, K Hibi, N Nyui, N Takagi, M Ishii

JOURNAL OF HYPERTENSION 16 S79 - S79 1998.6

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Downregulation of caveolin after chronic isoproterenol infusion in Mouse hearts

N Oka, K Asai, RK Kudej, JG Edwards, Y Toya, C Schwencke, DE Vatner, SF Vatner, Y Ishikawa

CIRCULATION 96 ( 8 ) 4175 - 4175 1997.10

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Isoform-dependent activation of adenylyl cyclase by proteolysis (vol 401, pg 223, 1997)

T Ebina, Y Toya, N Oka, J Kawabe, C Schwencke, Y Ishikawa

FEBS LETTERS 411 ( 2-3 ) 393 - 393 1997.7

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Isoform-specific interaction of adenylyl cyclase with caveolin.

C Schwencke, N Oka, Y Toya, Y Ishikawa

FASEB JOURNAL 11 ( 3 ) 1878 - 1878 1997.2

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Isoform-dependent activation of adenylyl cyclase by proteolysis

T Ebina, Y Toya, N Oka, J Kawabe, C Schwencke, Y Ishikawa

FEBS LETTERS 401 ( 2-3 ) 223 - 226 1997.1

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DOI： 10.1016/S0014-5793(96)01475-5

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Catecholamine and dopamine

S. Umemura, T. Ebina, Y. Toya, Y. Ishikawa, G. Yasuda

Nippon rinsho. Japanese journal of clinical medicine 55 ( 8 ) 1915 - 1922 1997

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AC-ALPHA, AN ENDOGENOUS INHIBITOR OF CARDIAC ADENYLYL-CYCLASE

JI KAWABE, T EBINA, CJ HOMCY, Y ISHIKAWA

CIRCULATION 92 ( 8 ) 2731 - 2731 1995.10

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Altered Platelet α_2-Adrenoceptors in Patients With Ischemic Heart Disease

UCHINO Kazuaki, UMEMURA Satoshi, OCHIAI Hisao, ISHIKAWA Yoshihiro, NIHEI Tohyoh, ISHII Masao

Japanese circulation journal 59 ( 10 ) 685 - 692 1995.9

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We evaluated the characteristics of platelet α_2-adrenoceptors in 12 patients with effort angina pectoris, 11 patients with variant angina pectoris and 11 normal control subjects. α_2-Adrenoceptors were quantified using a radioligand binding assay with radiolabelled rauwolscine, an α_2-selective antagonist. In addition, plasma norepinephrine concentration were measured by high performance liquid chromatography. The mean value of the maximal number of binding sites(B_<max>)in patients with effort angina(205.1±11.3 fmol/mg protein)was significantly lower than that in control subjects(293.0±10.2 fmol/mg protein). B_<max> did not differ between patients with variant angina(322.9±45.4 fmol/mg protein)and control subjects. There was no significant difference in the dissociation constant(K_d)among the 3 groups. The plasma norepinephrine concentration tended to be higher in patients with effort angina or variant angina than in normal controls, but this difference was not statistically significant. In addition, studies in another group of young volunteers(n=20)revealde a negative correlation(r=0.05, p<0.05)between the B_<max> of^3H-rauwolscine binding to platelets and the percent change in the plasma norepinephrine concentration when subjects moved from the supine to the standing position. This suggests a functional correlation between platelet α_2-adrenoceptors and those located at presynaptic sites. If platelet α_2-adrenoceptors correlate with presynaptic α_2-adrenoceptors, the current findings of decreased α_2-adrenoceptor density in platelets from patients with effort angina could represent attenuated negative feedback of norepinephrine by presynaptic α_2-adrenoceptors.

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DESENSITIZATION OF ADENYLYLCYCLASE BY PHOSPHORYLATION

G IWAMI, J KAWABE, T EBINA, S ISMAIL, PJ CANNON, CJ HOMCY, Y ISHIKAWA

CIRCULATION 90 ( 4 ) 413 - 413 1994.10

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DIFFERENTIAL ACTIVATION OF ADENYLYL-CYCLASE BY PROTEIN-KINASE-C ISOENZYMES (VOL 269, PG 16554, 1994)

JI KAWABE, G IWAMI, T EBINA, S OHNO, T KATADA, Y UEDA, CJ HOMCY, Y ISHIKAWA

JOURNAL OF BIOLOGICAL CHEMISTRY 269 ( 36 ) 22912 - 22912 1994.9

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PROTEIN-KINASE-C REGULATES ADENYLYLCYCLASE CATALYTIC ACTIVITY IN AN ISOENZYME-SPECIFIC MANNER

J KAWABE, G IWAMI, T EBINA, S ISMAIL, CJ HOMCY, Y ISHIKAWA

FASEB JOURNAL 8 ( 7 ) A1388 - A1388 1994.4

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INVIVO GENERATION OF AN ADENYLYLCYCLASE ISOFORM WITH A HALF-MOLECULE MOTIF

S KATSUSHIKA, J KAWABE, CJ HOMCY, Y ISHIKAWA

JOURNAL OF BIOLOGICAL CHEMISTRY 268 ( 4 ) 2273 - 2276 1993.2

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CHARACTERIZATION OF NOVEL MEMBERS OF CARDIAC ADENYLYL CYCLASE FAMILY - MESSENGER-RNA LEVELS PARALLEL THE DEVELOPMENT OF HEART-FAILURE

Y ISHIKAWA, S KATSUSHIKA, J KAWABE, DE VATNER

CIRCULATION 86 ( 4 ) 767 - 767 1992.10

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REDUCED STEADY-STATE MESSENGER-RNA LEVELS OF CARDIAC ADENYLYL CYCLASE (AC) PARALLELS THE DEVELOPMENT OF HEART-FAILURE

Y ISHIKAWA, S KATSUSHIKA, L CHEN, K KIUCHI, K KOMAMURA, RP SHANNON, DE VATNER, SF VATNER, CJ HOMCY

CLINICAL RESEARCH 40 ( 2 ) A220 - A220 1992.4

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-P105-LOCALIZATION OF ALPHA 1 AND ALPHA 2 ADRENOCEPTORS IN THE HUMAN KIDNEY : Hypertension : FREE COMMUNICATIONS(III) : PROCEEDINGS OF THE 53th ANNUAL SCIENTIFIC MEETING OF THE JAPANESE CIRCULATION SOCIETY

Minamisawa Kohsuke, Umemura Satoshi, Hirawa Nobuhito, Hayashi Shuuichi, Toya Yoshiyuki, Ishikawa Yoshihiro, Yasuda Gen, Ishii Masao

Japanese circulation journal 53 ( 6 ) 669 - 669 1989.6

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HUMAN ATRIAL NATRIURETIC PEPTIDE INHIBITED CELLULAR CYCLIC-AMP LEVELS IN MICRODISSECTED HUMAN GLOMERULI

Y TOYA, S UMEMURA, N HIRAWA, Y ISHIKAWA, G YASUDA, K MINAMIZAWA, S HAYASHI, M ISHII

JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 52 ( 9 ) 1046 - 1047 1988.9

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ALPHA-2-ADRENOCEPTOR STIMULATION INHIBITED CELLULAR CYCLIC-AMP LEVELS IN MICRODISSECTED HUMAN GLOMERULI

N HIRAWA, S UMEMURA, Y TOYA, K MINAMIZAWA, G YASUDA, Y ISHIKAWA, S HAYASHI, M ISHII

JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 52 ( 9 ) 973 - 973 1988.9

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Applicant：株式会社IHI, 石川義弘

Application no：特願2011-131239 Date applied：2011.6

Announcement no：特開2013-001646 Date announced：2013.1

Patent/Registration no：特許第5873656号 Date issued：2016.1

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金属サレン錯体化合物、局所麻酔薬剤及び抗悪性腫瘍薬剤

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2011-131239 Date applied：2011.6

Announcement no：特開2013-001646 Date announced：2013.1

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蛍光色素材料及びその使用方法

石川義弘, 江口晴樹

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Applicant：株式会社IHI, 石川義弘

Application no：特願2012-518218 Date applied：2011.5

Patent/Registration no：特許第5554408号 Date issued：2014.6

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蛍光色素材料及びその使用方法

石川義弘, 江口晴樹

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Applicant：株式会社IHI, 石川義弘

Application no：JP2011002651 Date applied：2011.5

Announcement no：WO2011-151978 Date announced：2011.12

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抗脳腫瘍薬剤

石川義弘, 江口晴樹

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Applicant：株式会社IHI, 石川義弘

Application no：特願2012-512639 Date applied：2011.4

Patent/Registration no：特許第5680065号 Date issued：2015.1

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抗脳腫瘍薬剤

石川義弘, 江口晴樹

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Applicant：株式会社IHI, 石川義弘

Application no：JP2011002118 Date applied：2011.4

Announcement no：WO2011-135784 Date announced：2011.11

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金属サレン錯体誘導体及びその製造方法

石川義弘, 江口晴樹, 佐藤裕

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Applicant：株式会社IHI, 石川義弘

Application no：特願2012-509317 Date applied：2011.4

Patent/Registration no：特許第5736367号 Date issued：2015.4

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金属サレン錯体誘導体及びその製造方法

石川義弘, 江口晴樹, 佐藤裕

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Applicant：株式会社IHI, 石川義弘

Application no：JP2011002056 Date applied：2011.4

Announcement no：WO2011-125331 Date announced：2011.10

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金属サレン錯体化合物

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2011-040233 Date applied：2011.2

Announcement no：特開2012-176905 Date announced：2012.9

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自己磁性金属サレン錯体化合物

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2011-030056 Date applied：2011.2

Announcement no：特開2012-167067 Date announced：2012.9

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ドラッグデリバリー制御装置

石川義弘, 江口晴樹, 原正一

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Applicant：株式会社IHI, 石川義弘

Application no：特願2011-547329 Date applied：2010.12

Patent/Registration no：特許第5372178号 Date issued：2013.9

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磁石体及び磁石体を用いたドラッグデリバリー制御装置

石川義弘, 江口晴樹, 原正一

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Applicant：株式会社IHI, 石川義弘

Application no：JP2010007516 Date applied：2010.12

Announcement no：WO2011-077750 Date announced：2011.6

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金属サレン錯体化合物及びその製造方法

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2010-285075 Date applied：2010.12

Announcement no：特開2012-131737 Date announced：2012.7

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自己磁性金属サレン錯体化合物

石川義弘, 江口晴樹

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Applicant：株式会社IHI, 石川義弘

Application no：特願2010-539038 Date applied：2009.11

Patent/Registration no：特許第5513405号 Date issued：2014.4

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自己磁性金属サレン錯体化合物

石川義弘, 江口晴樹

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Applicant：株式会社IHI, 石川義弘

Application no：IB2009007525 Date applied：2009.11

Announcement no：WO2010-058280 Date announced：2010.5

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鉄サレン錯体

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2009-264213 Date applied：2009.11

Announcement no：特開2010-043125 Date announced：2010.2

Patent/Registration no：特許第5461968号 Date issued：2014.1

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鉄サレン錯体

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2009-264213 Date applied：2009.11

Announcement no：特開2010-043125 Date announced：2010.2

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鉄サレン錯体

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2008-298128 Date applied：2008.11

Announcement no：特開2009-173631 Date announced：2009.8

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鉄サレン錯体

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2008-298128 Date applied：2008.11

Announcement no：特開2009-173631 Date announced：2009.8

Patent/Registration no：特許第4446489号 Date issued：2010.1

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薬、薬の誘導装置、磁気検出装置及び薬の設計方法

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2008-280773 Date applied：2008.10

Announcement no：特開2009-108068 Date announced：2009.5

J-GLOBAL

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医療用チューブ又は薬剤の誘導システム

石川義弘, 江口晴樹

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Applicant：石川義弘, 株式会社IHI

Application no：特願2008-160794 Date applied：2008.6

Announcement no：特開2010-000202 Date announced：2010.1

Patent/Registration no：特許第5723081号 Date issued：2015.4

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医療用チューブ又は薬剤の誘導システム

石川義弘, 江口晴樹

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Applicant：石川義弘, 株式会社IHI

Application no：特願2008-160794 Date applied：2008.6

Announcement no：特開2010-000202 Date announced：2010.1

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抗体又は抗原の定量方法

石川義弘, 江口晴樹

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Applicant：石川義弘, 株式会社IHI

Application no：特願2008-137888 Date applied：2008.5

Announcement no：特開2009-287949 Date announced：2009.12

Patent/Registration no：特許第5408905号 Date issued：2013.11

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磁性体化合物のスクリーニング方法

石川義弘, 江口晴樹

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Applicant：石川義弘, 株式会社IHI

Application no：特願2008-137885 Date applied：2008.5

Announcement no：特開2009-287948 Date announced：2009.12

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磁性体化合物のスクリーニング方法

石川義弘, 江口晴樹

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Applicant：石川義弘, 株式会社IHI

Application no：特願2008-137885 Date applied：2008.5

Announcement no：特開2009-287948 Date announced：2009.12

Patent/Registration no：特許第5339777号 Date issued：2013.8

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抗体又は抗原の定量方法

石川義弘, 江口晴樹

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Applicant：石川義弘, 株式会社IHI

Application no：特願2008-137888 Date applied：2008.5

Announcement no：特開2009-287949 Date announced：2009.12

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スイッチング素子

石川義弘, 江口晴樹

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Applicant：石川義弘, 株式会社IHI

Application no：特願2008-137895 Date applied：2008.5

Announcement no：特開2009-289799 Date announced：2009.12

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鉄サレン錯体、磁性を有する薬剤、薬剤の誘導システム、並びに磁気検出装置

石川義弘, 江口晴樹

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Applicant：石川義弘, 株式会社IHI

Application no：特願2008-125202 Date applied：2008.5

Announcement no：特開2009-274962 Date announced：2009.11

J-GLOBAL

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磁性を有する薬剤、薬剤の誘導システム、並びに磁気検出装置

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2008-105912 Date applied：2008.4

Announcement no：特開2009-256232 Date announced：2009.11

J-GLOBAL

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磁性を有する薬剤、薬剤の誘導システム、並びに磁気検出装置

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2008-105917 Date applied：2008.4

Announcement no：特開2009-256233 Date announced：2009.11

J-GLOBAL

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磁性を有する薬剤、薬剤の誘導システム、並びに磁気検出装置

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2008-038458 Date applied：2008.2

Announcement no：特開2009-196912 Date announced：2009.9

Patent/Registration no：特許第5433155号 Date issued：2013.12

J-GLOBAL

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磁性を有する薬剤、薬剤の誘導システム、並びに磁気検出装置

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2008-038502 Date applied：2008.2

Announcement no：特開2009-196914 Date announced：2009.9

J-GLOBAL

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磁性を有する薬剤

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2008-038502 Date applied：2008.2

Announcement no：特開2009-196914 Date announced：2009.9

Patent/Registration no：特許第5325427号 Date issued：2013.7

J-GLOBAL

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磁性を有する薬剤、薬剤の誘導システム、並びに磁気検出装置

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2008-038458 Date applied：2008.2

Announcement no：特開2009-196912 Date announced：2009.9

J-GLOBAL

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磁性を有する薬剤、薬剤の誘導システム、並びに磁気検出装置

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2008-038476 Date applied：2008.2

Announcement no：特開2009-196913 Date announced：2009.9

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MRIシステム

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2007-316941 Date applied：2007.12

Announcement no：特開2008-150368 Date announced：2008.7

Patent/Registration no：特許第4279335号 Date issued：2009.3

J-GLOBAL

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薬、薬の誘導装置、磁気検出装置及び薬の設計方法

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2007-316941 Date applied：2007.12

Announcement no：特開2008-150368 Date announced：2008.7

J-GLOBAL

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土被り部用高耐力アンカー

鈴木春男, 吉田泰則, 庄司勇蔵, 石川義弘

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Applicant：東京製綱株式会社

Application no：特願2007-250440 Date applied：2007.9

Announcement no：特開2009-079434 Date announced：2009.4

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磁性薬誘導システム

石川義弘, 江口晴樹

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Applicant：株式会社IHI, 石川義弘

Application no：特願2008-522625 Date applied：2007.6

Patent/Registration no：特許第5378792号 Date issued：2013.10

J-GLOBAL

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薬、薬の誘導装置、磁気検出装置及び薬の設計方法

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2007-170909 Date applied：2007.6

Announcement no：特開2007-314544 Date announced：2007.12

J-GLOBAL

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演算装置及び局所治療薬

江口晴樹, 石川義弘

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Applicant：株式会社IHI, 石川義弘

Application no：特願2007-170909 Date applied：2007.6

Announcement no：特開2007-314544 Date announced：2007.12

Patent/Registration no：特許第4279330号 Date issued：2009.3

J-GLOBAL

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薬、薬の誘導装置、磁気検出装置及び薬の設計方法

石川義弘, 江口晴樹

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Applicant：株式会社IHI, 石川義弘

Application no：JP2007063011 Date applied：2007.6

Announcement no：WO2008-001851 Date announced：2008.1

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薬、薬の誘導装置、体内動態検知器及び薬の設計方法

江口晴樹, 石川義弘, 谷垣勝己

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Applicant：石川義弘

Application no：特願2006-301564 Date applied：2006.11

Announcement no：特開2008-115129 Date announced：2008.5

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抗がん薬

江口晴樹, 石川義弘, 谷垣勝己

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Applicant：株式会社IHI, 公立大学法人横浜市立大学

Application no：特願2006-301564 Date applied：2006.11

Announcement no：特開2008-115129 Date announced：2008.5

Patent/Registration no：特許第5167481号 Date issued：2013.1

J-GLOBAL

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磁性材料、磁性材料の誘導装置及び磁性材料の設計方法

江口晴樹, 石川義弘, 谷垣勝己

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Applicant：石川義弘

Application no：特願2006-300604 Date applied：2006.11

Announcement no：特開2008-117969 Date announced：2008.5

J-GLOBAL

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磁性材料、磁性材料の誘導装置及び磁性材料の設計方法

江口晴樹, 石川義弘, 谷垣勝己

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Applicant：株式会社IHI, 公立大学法人横浜市立大学

Application no：特願2006-300604 Date applied：2006.11

Announcement no：特開2008-117969 Date announced：2008.5

Patent/Registration no：特許第4774536号 Date issued：2011.7

J-GLOBAL

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薬、薬の誘導装置、磁気検出装置及び薬の設計方法

江口晴樹, 石川義弘

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Applicant：石川島播磨重工業株式会社, 石川義弘

Application no：特願2006-177971 Date applied：2006.6

Announcement no：特開2007-091710 Date announced：2007.4

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ヒアルロン酸合成促進による内膜肥厚及びその利用

南沢享, 横山詩子, 石川義弘

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Applicant：公立大学法人横浜市立大学

Application no：特願2005-299288 Date applied：2005.10

Announcement no：特開2007-106698 Date announced：2007.4

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評価対象化合物の活性度評価方法

江口晴樹, 石川義弘, 岩坪耕策

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Applicant：石川島播磨重工業株式会社, 石川義弘

Application no：特願2005-251189 Date applied：2005.8

Announcement no：特開2007-064795 Date announced：2007.3

J-GLOBAL

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評価対象化合物の薬剤活性度評価方法

江口晴樹, 石川義弘, 岩坪耕策

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Applicant：株式会社IHI, 石川義弘

Application no：特願2005-251189 Date applied：2005.8

Announcement no：特開2007-064795 Date announced：2007.3

Patent/Registration no：特許第4216277号 Date issued：2008.11

J-GLOBAL

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サブタイプ選択的アデニル酸シクラーゼ活性化剤

永井昌史, 斉藤清一, 倉持浩, 恩田健, 石川義弘

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Applicant：日本化薬株式会社

Application no：特願2001-154039 Date applied：2001.5

Announcement no：特開2002-348283 Date announced：2002.12

J-GLOBAL

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サブタイプ選択的アデニル酸シクラーゼ活性化剤

永井昌史, 斉藤清一, 倉持浩, 恩田健, 石川義弘

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Applicant：日本化薬株式会社

Application no：特願2001-154039 Date applied：2001.5

Announcement no：特開2002-348283 Date announced：2002.12

Patent/Registration no：特許第4722325号 Date issued：2011.4

J-GLOBAL

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アデニル酸シクラーゼ5型阻害剤

永井昌史, 恩田健, 倉持浩, 石川義弘

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Applicant：日本化薬株式会社

Application no：特願2001-153954 Date applied：2001.5

Announcement no：特開2002-338467 Date announced：2002.11

Patent/Registration no：特許第4723115号 Date issued：2011.4

J-GLOBAL

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アデニル酸シクラーゼ5型阻害剤

永井昌史, 恩田健, 倉持浩, 石川義弘

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Applicant：日本化薬株式会社

Application no：特願2001-153954 Date applied：2001.5

Announcement no：特開2002-338467 Date announced：2002.11

J-GLOBAL

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心臓のアデニリルシクラーゼのクローニングおよび特性決定

石川義弘

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Applicant：アメリカン・サイアナミド・カンパニー

Application no：特願平4-331027 Date applied：1992.11

Announcement no：特開平5-276961 Date announced：1993.10

J-GLOBAL

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心臓アデニリルシクラーゼのクローニングおよび特性決定

石川義弘

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Applicant：アメリカン・サイアナミド・カンパニー

Application no：特願平4-250397 Date applied：1992.8

Announcement no：特開平5-260977 Date announced：1993.10

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Awards

Fellow

2014 European Society of Cardiology

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Fellow

2010 Royal Society of Medicine, England

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Fellow

2004 American College of Cardiology

yoshihiro ishikawa

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Fellow

2000 American College of Physicians

yoshihiro ishikawa

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Established Investigator Award

1998 American Heart Association

yoshihiro ishikawa

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Fellow

1993 American Heart Association

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Yokohama Medical Award

1998 Yokohama City University Medical Association

yoshihiro ishikawa

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Okamoto Award

1998 Japan Vascular Disease Research Foundation

yoshihiro ishikawa

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Fellow

1995 American Heart Association

yoshihiro ishikawa

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Medical Science Achievement Award

1993 Lederle Laboratories

yoshihiro ishikawa

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Scholarship

1982 International Rotary Foundation Rotary Foundation Scholarship

yoshihiro ishikawa

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Research Projects

Molecular mechanism of magnetic sensor in pancreatic cancer cells

Grant number：22H03926 2022.4 - 2025.3

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

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Grant amount：\17420000 （ Direct Cost: \13400000 、 Indirect Cost：\4020000 ）

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Regulation of cardiac function by the autonomic nervous system

Grant number：19H03657 2019.4 - 2022.3

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B) Grant-in-Aid for Scientific Research (B)

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Grant amount：\17420000 （ Direct Cost: \13400000 、 Indirect Cost：\4020000 ）

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Autonomic regulation of cardiac function

Grant number：16H05300 2016.4 - 2019.3

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B) Grant-in-Aid for Scientific Research (B)

Ishikawa Yoshihiro

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Grant amount：\17290000 （ Direct Cost: \13300000 、 Indirect Cost：\3990000 ）

The sympathetic nervous system is a major mechanism of regulating cardiac function together with the Frank Starling mechanism. Catecholamine is a neurotramsmitter molecule of the sympathetic nervous system, and activates adenylyl cyclase to produce cAMP. This second messenger activates protein kinase A, however, recent studies have identified Epac as another target enzyme. Epac is directly activated by cAMP, and activaes Rap and other G protein-related molecules within the regulation of cellular function. In the current research project, we have compared the role of Epac with that of protein kinase A, and found its regulation within the cAMP network that regulates cardiac function and the development of heart failure.

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Molecular mechanism of the heart by the autonomic nervous system

Grant number：21390246 2012

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B) Grant-in-Aid for Scientific Research (B)

ISHIKAWA Yoshihiro, SATO Motohiko, OKUMURA Satoshi

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Grant amount：\17810000 （ Direct Cost: \13700000 、 Indirect Cost：\4110000 ）

Adenylyl cyclase is a membrane bound enzyme that catalyzes the production of cAMP. Epac is a new molecule, which is regulated by cAMP independently from PKA. In the model of Epac overexpression, we found an interesting cross talk between cytokine and cAMP signal.

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Establishment of Integrative Multi-level Systems Biology and its Applications

Grant number：22136001 2010.4 - 2016.3

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area) Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)

KURACHI YOSHIHISA, INOUE Ryuji, YAMASHITA Fumiyoshi, SUZUKI Hiroshi, KITANO Hiroaki, OHTSUKI Sumio, AMANO Akira, KINOSHITA Kengo, HARI Yoshiyuki, MAKITA Naomasa, ISHIKAWA Yoshihiro, HONJO Haruo, NAKAZAWA Kazuo, OKUNO Yasushi, KUSUHARA Hiroyuki, KAGECHIKA Hiroyuki

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Grant amount：\64220000 （ Direct Cost: \49400000 、 Indirect Cost：\14820000 ）

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GTP結合蛋白によるcAMPシグナルの制御メカニズム

Grant number：18057018 2006 - 2007

日本学術振興会科学研究費助成事業特定領域研究特定領域研究

石川義弘, 南沢享, 奥村敏, 佐藤元彦

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Grant amount：\6400000 （ Direct Cost: \6400000 ）

cAMPはG結合タンパク質によって制御される代表的な細胞内シグナル系である。カテコラミン受容体などにアゴニストが結合すると刺激性G蛋白質の活性化を引き起こし,これがアデニル酸シクラーゼの活性化とcAMP依存性キナーゼ(PKA)の活性化を引き起こす。PKAは細胞内の多数の蛋白をリン酸化することにより機能変化をもたらし細胞機能を制御している。従来cAMPの標的分子の主体はPKAであるとされてきたが,近年Epac(Exchange Protein directly Activated by cAMP)と呼ばれるグアニンヌクレオチド交換因子(GEF)がcAMPによって直接活性化されることが証明された。EpacはRapなどのG蛋白質活性を制御することが知られているが,その詳細は明らかでない。本申請ではこの新規G蛋白質活性調節分子であるEpacのcAMPシグナルにおける役割を、心血管系組織を中心に検討した。
心血管系は成長段階とともに細胞蛋白発現量あるいはサブタイプ比率がダイナミックに変化することが知られており,この変化が発育段階における心機能調節と密接な関連をもつとされる。Epacには組織分布の異なる2つのサブタイプが存在するが,これらの発現が発育段階に応じてどのように変化するのかを心臓,肺,腎臓,脳において検討したところ,発育段階および臓器によって特徴的な変化をしめすことがわかった。このことはEpacが臓器の発育に重要な役割を果たす可能性を意味する。
さらに我々は過大発現マウスを用いた実験の結果から,心筋炎などの心機能低下が知られているが,Epacがサイトカインシグナルにおいて重要な役割を果たすことがわかってきた。Epac過大発現マウスにLPS刺激による心不全を起こし,心機能を測定したところ,野生種に比較して著名に心機能の低下が予防できることがわかった。このことはEpacが心機能維持に大切な役割を果たすことを意味する。
以上の結果から,心血管系においてGTP結合蛋白はcAMPシグナルの調節を受け,心機能などの維持に重要な役割を果たすと考えられる。

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Molecular mechanism of magnetic sensor in pancreatic cancer cells

Grant number：23K25180 2022.4 - 2025.3

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

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Grant amount：\17420000 （ Direct Cost: \13400000 、 Indirect Cost：\4020000 ）

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How to predict the collapse of homeostasis in circulatory regulation

Grant number：18KT0073 2018.7 - 2021.3

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C) Grant-in-Aid for Scientific Research (C)

ISHIKAWA Yoshihiro

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Grant amount：\4420000 （ Direct Cost: \3400000 、 Indirect Cost：\1020000 ）

Sympathetic nervous system is a major mechanism of regulating cardiac function. It is mostly made of cAMP signal that is essential for intracellular signal in the heart. In this study, we have addressed mathematical and physical characteristics of cAMP and calcium signal in the heart, which are known to play a major role in regulating cardiac arrythmia and thus cardiac homeostasis. In particular, overactivation of the sympathetic nervous system and pressure overload in congestive heart failure are major reasons to induce cardiac pathophysiology. We have analyzed spacial and sequential role of gene expression as well as its deletion, that leads to altered enzymatic activity. We found that pharmacologically they are important at the level of both cell and body.

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Development of magnetic antibiotics

Grant number：16K15205 2016.4 - 2017.3

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research Grant-in-Aid for Challenging Exploratory Research

ISHIKAWA Yoshihiro

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Grant amount：\3640000 （ Direct Cost: \2800000 、 Indirect Cost：\840000 ）

The method for evaluating metal material has been applied to pharmaceutical compounds. Accordingly, we have found compounds with strong magnetism, which also has toxicity. With chemical researchers, we have synthesized magnetic compounds with less toxicity. In this research project, we have examined this compound and studied its application for magnetizing antibiotic compounds. We have synthesized ampicillin which has been magnetized by this compounds. We have found that this magnetized ampicillin was indeed weakly magnetic. Our findings suggest that it is feasible to magnetize antibiotics. In the future study it will be needed to evaluate antibiotic activity of magnetized ampicillin and its guided delivery by magnet.

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Development of new antiarrhythmic drugs alternative to beta blocker therapy

Grant number：15K18973 2015.4 - 2019.3

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B) Grant-in-Aid for Young Scientists (B)

Suita Kenji, ISHIKAWA Yoshihiro, OKUMURA Satoshi

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Grant amount：\4030000 （ Direct Cost: \3100000 、 Indirect Cost：\930000 ）

Excessive and chronic activation of sympathetic beta-adrenergic receptor (β-AR) signal are known to be a trigger of arrhythmias. In this study, we focus on the cardiac subtype of adenylate cyclase (AC) and exchanged protein directly activated by cAMP (Epac), a cAMP target protein, that mediates the β-AR signaling. We used the gene knockout mice to determine the role of both factors in arrhythmogenesis. Further, antiarrhythmic effect and adverse effects on cardiac function of inhibitors selective for cardiac AC and Epac1 subtypes were compared with a β-blocker. As a result, arrhythmia onset was significantly suppressed in AC5 and Epac1 knockout mice as compared to control mice. In addition, it has been clarified that inhibitors of both molecules prevented arrhythmias without deteriorating heart function as observed in β-blocker-treated mice.

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Three-dimensional multilayers of smooth muscle cells as a new experimental model for vascular biology

Grant number：24659100 2012.4 - 2014.3

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research Grant-in-Aid for Challenging Exploratory Research

YOKOYAMA Utako, ISHIKAWA Yoshihiro, ICHIKAWA Yasuhiro

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Grant amount：\3900000 （ Direct Cost: \3000000 、 Indirect Cost：\900000 ）

Elastic fiber formation is disrupted with age and by health conditions including aneurysms and atherosclerosis. Despite considerable progress in the understanding of elastogenesis using the planar culture system and genetically modified animals, it remains difficult to restore elastic fibers in diseased vessels. To further study the molecular mechanisms, we created in vitro three-dimensional vascular constructs. Three-dimensional cellular multilayers (3DCMs), which consisted of seven layers of neonatal rat aortic SMCs cultured in 1% fetal bovine serum in DMEM medium, exhibited layered elastic fibers and differentiated smooth muscle cell phenotype within seven days of being in a static culture condition. Furthermore, infiltration of THP-1-derived macrophages decreased the surrounding elastic fiber formation in 3DCMs. 3DCMs may offer a new experimental vascular model to explore pharmacological therapeutic strategies for abnormal vascular remodeling.

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Molecular mechanisms of ductus arteriosus closure

Grant number：23390277 2011.4 - 2014.3

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B) Grant-in-Aid for Scientific Research (B)

MINAMISAWA Susumu, YOKOYAMA Utako, GODA Nobuhito, ISHIKAWA Yoshihiro, NAKAMURA Tomoyuki, SUGIMOTO Yukihiko, AOKI Hiroki

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Grant amount：\19110000 （ Direct Cost: \14700000 、 Indirect Cost：\4410000 ）

The ductus arteriosus (DA) is an essential fetal artery that closes immediately after birth. However, the molecular mechanisms remain unknown, especially its vascular remodeling. We found that 1) prostaglandin E2 (PGE2) -EP4 signaling decreased elastic fiber formation through degradation of the cross-linking enzyme lysyl oxidase, and that 2) NFkB signal could be activated by PGE2-EP4 stimulation via cAMP-independent pathway, and that 3) endothelial cells of the DA exhibited a unique gene profile involved in the regulation of DA-specific morphology and function. These novel findings regarding DA vascular remodeling could open a possibility to innovate a new therapeutic strategy for the regulation of DA closure.

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心臓型アデニル酸シクラーゼとＥｐａｃを治療標的にした新しいベータ遮断薬の開発

Grant number：11F01418 2011 - 2013

日本学術振興会科学研究費助成事業特別研究員奨励費特別研究員奨励費

石川義弘, 金美花

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Grant amount：\1400000 （ Direct Cost: \1400000 ）

cAMP産生酵素であるアデニル酸シクラーゼは、神経伝達物質をはじめとして各種ホルモン受容体の標的酵素として、細胞内においてセカンドメッセンジャーシグナルを調節する酵素である。心臓のカテコラミン受容体の主体をなすβ受容体の阻害剤であるβ遮断剤は、心臓での交感神経刺激を抑制する薬剤として、心不全や不整脈の治療薬として多方面で使用されている。しかしながら肺や中枢にも発現するために、肺気腫や気管支ぜんそく患者においては、使用禁忌である。そこで心臓のみβ遮断剤が作用するようにすれば、この副作用は軽減される。アデニル酸シクラーゼの多数のサブタイプのうち、心臓型と呼ばれる5型サブタイプは、心臓特異的に発現することが知られている。従ってこの5型サブタイプを選択的に抑制することが出来れば、そあ下流因子のシグナルも含めて抑制できる。本研究では、5型サブタイプの選択抑制が、下流の酵素シグナルであるEpac系の抑制変化を起こしうるかを、遺伝子操作動物との関連において検討した。このためにマウスの心房ページングを、食道ペーシングにおいて施行するモデルを作成し、心臓不整脈の亢進モデルを確立し、これまでの短時間モデルの欠点を克服することを目的とした。電極カテーテルを用いて様々な誘発特性の最適化をおこなった。条件の検討においては、マウスの管理状態、付随する条件検討を中心に行い、カテコラミン誘発性刺激を負荷したところ、ノルアドレナリンの刺激を事前に加えることにより、マウスの不整脈の誘発が亢進し、持続時間が亢進することが解った。この変化は、細胞内のセカンドメッセンジャーシグナルの調節によって変化することが解明された。我々の検討結果から、マウスの不整脈の性状は、・副交感および交感神経刺激の状態によって大きく作用される可能性が示唆され、不整脈の誘発には重要であることが解った。

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カベオリンペプチドを用いた糖尿病治療への応用

2009

産学が連携した研究開発成果の展開研究成果展開事業地域事業地域イノベーション創出総合支援事業シーズ発掘試験

石川義弘

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Authorship：Principal investigator

糖尿病はインシュリン作用の欠乏によっておこる代表的代謝疾患であり、インスシュリン補充が理想的な治療法である。我々はカベオリンと呼ばれる膜構成蛋白に、内因性インシュリン増強作用があることを見出した。さらに30アミノ酸からなる短いペプチドのみでインシュリン効果の増強に十分であることも見出した。このカベオリンペプチドを用いて、全く作用機序の新しい安全で効果的な糖尿病治療薬の開発を試みる。

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GTP結合蛋白によるcAMPシグナルの制御

Grant number：20054016 2008 - 2009

日本学術振興会科学研究費助成事業特定領域研究特定領域研究

石川義弘, 佐藤元彦, 奥村敏

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Grant amount：\5200000 （ Direct Cost: \5200000 ）

Epacは近年になって発見されたcAMPシグナルの構成因子であり、G蛋白質の活性調節に重要な役割を果たすと推測されている。我々のグループは心血管系におけるEpacの役割を中心に検討することを計画した。血管平滑筋の遊走は、動脈管閉塞などの生理的、あるいは動脈硬化病変における病的な血管内空閉塞などに重要な役割を果たすことが知られているが、血管平滑筋の遊走制御にEpac発現の亢進が見られ、さらにEpac過大発現によって血管平滑筋の遊走が亢進することが確認された。その一方でPKAの過大発現ではこのような現象は見られず、cAMPシグナルにおけるEpacの果たす役割の重要性が確認された。さらに我々はEpacを過大発現させたモデル、欠損させたモデルを作製したところ、欠損モデルにおいて定常状態における軽度心機能低下が見られた。また過大発現モデルにおいては、Epac1過大発現で心機能に変化は見られないが、LPS刺激による敗血症発症に際して、野生型で見られる心機能低下がおこらなかった。このことはEpac発現は心機能保護に働く可能性が示唆された。この分子メカニズムについては、TLRシグナルとEpacとのクロストークの存在が考えられた。とりわけSOCSシグナルの制御にEpacが重要な役割を果たすことが推測された。以上より、Epacは心筋保護作用を通じて、また細胞遊走を制御することによって、心血管系における重要な役割を果たすと考えられる。

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Molecular mechanism of autonomic regulation of cardiac function

Grant number：19390217 2007 - 2008

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B) Grant-in-Aid for Scientific Research (B)

ISHIKAWA Yoshihiro, SATO Motohiko, OKUMURA Satoshi, MINAMISAWA Susumu

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Grant amount：\18720000 （ Direct Cost: \14400000 、 Indirect Cost：\4320000 ）

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Molecular mechanisms for cardiac regulation by the autonomic nervous system

Grant number：17390234 2005 - 2006

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B) Grant-in-Aid for Scientific Research (B)

ISHIKAWA Yoshihiro, MINAMISAWA Susumu, SATO Motohiko, OKUMURA Satoshi, IWATSUBO Kousaku

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Grant amount：\15300000 （ Direct Cost: \15300000 ）

Sympathetic nervous system is a major mechanism of regulating cardiac function. Catecholamines released from the synaptic terminal bind to catecholamine receptors, leading to the activation of the stimulatory G protein and then adenylyl cyclase, leading to increased cardiac contractility and heart rate. There are at least 9 subtypes for adenylyl cyclase; type 5 is known to be the major subtype expressed in the heart. This isoform has been known to be developmentally regulated; its expression is relatively low at birth, but increased with aging. We have demonstrated that there are multiple mechanism to regulate this adenylyl cyclase subtype through distinct mechanisms of regulation. In the current research, we have investigated the role of this adenylyl cyclase subtype in not only regulating cardiac function but regulating and inducing cardiac myocyte apoptosis. We examined its role under chronic catecholamine stimulation. In order to examine the role of this adenylyl cyclase subtype, we developed a mouse line in which the expression of this subtype was deleted. Basal cardiac function was relatively maintained in AC5KO, however, after chronic isoproterenol infusion by the use of osmotic minipump, cardiac function in wild type mice deteriorated significantly while that in AC5KO remained relatively conserved. When the number of apoptotic cardiac myocytes were counted, we found that the number was significantly decreased in AC5KO. Furthermore, the activation of Ala was significantly increased in AC5KO. These findings have suggested that the deletion of type 5 adenylyl cyclase plays a beneficial role in protecting the heart from chronic catecholamine stress. Together with recent development of compounds that can inhibit this adenylyl cyclase subtype in a subtype-specific manner, it is tentative to propose that the use of such type 5 adenylyl cyclase inhibitor may serve as an alternate to protect the heart under various pathophysiological condition where catecholamine stress is increased.

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細胞膜構造が成長刺激を引き起こしうるか?

Grant number：17659097 2005

日本学術振興会科学研究費助成事業萌芽研究萌芽研究

石川義弘

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Grant amount：\3200000 （ Direct Cost: \3200000 ）

我々は、インシュリン受容体が存在する細胞膜構造自体に、イシシュリン信号を刺激するメカニズムが存在することを検討した。さらにその細胞膜構造の主要構成蛋白であるカベオリンに、インシュリン受容体刺激作用があり、カベオリン遺伝子導入が糖尿病の病態生理の改善に役に立つことを実証することが目的であった。
膵臓から放出されたインシュリンは、細胞膜表面上のインシュリン受容体に結合し、受容体の自己リン酸化を引き起こすとともに、IRSと結合してリン酸化する。IRSはドッキング蛋白として下流の信号分子をリクルートするとともに細胞内シグナル連鎖を展開していく。これが従来考えられてきたインシュリンシグナルであり、インシュリンとインシュリン受容体の細胞膜表面における結合は、細胞内シグナルを開始するのに必要かつ十分であり,膜構造は信号蛋白を,単純に安定させるためだけと考えられてきた。
我々はカベオリンをアデノウイルスを用いて、高脂肪食により肥満と糖尿病を誘発させたマウスの肝臓に過大発現させたところ、コントロール群に比較して有意に血糖値の低下と経口糖負荷試験結果の改善が見られた。インシュリン感受性の著名な亢進もカベオリン遺伝子導入によってみられた。以上の所見から、カベオリンはインシュリンシグナルに重要な働きを示すのみならず、遺伝子導入によって糖代謝の改善を図ることが可能であることが示唆された。これは将来の遺伝子治療への応用の可能性を意味する。

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細胞内酵素機能障害としてのパーキンソン病の研究

Grant number：17025034 2005

日本学術振興会科学研究費助成事業特定領域研究特定領域研究

石川義弘, 南沢享, 岩坪耕策, 岩本彩男

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Grant amount：\2900000 （ Direct Cost: \2900000 ）

従来パーキンソン病の病態は、黒質線条体系におけるドーパミン枯渇によるシグナルの低下として、神経伝達物質あるいは受容体調節の異常として検討されてきたが、線条体細胞内の酵素機能異常としての可能性がある。線条体ドーパミン受容体シグナルの標的酵素としてアデニル酸シクラーゼがあげられるが、同酵素には9種類のサブタイプが存在し、線条体には同部位に特異的に発現する5型サブタイプが知られている。
我々の開発した5型ノックアウト動物では、線条体に限局したcAMPシグナルの欠損がみられ、協調運動の障害などの運動機能障害がみられ、さらにヒトパーキンソン病治療薬投与によって症状の改善がみられることから、パーキンソン病の原因としてのアデニル酸シクラーゼの酵素機能障害が考えられる。本申請ではその酵素機能異常とパーキンソン病の関連を明らかにするとともに、培養線条体細胞における同酵素の役割を検討した。
1.数ヶ月に及ぶ試行錯誤の結果、2週令マウスより得られた線条体細胞の安定した初代培養に成功した。コラゲナーゼなどの酵素処理時間の調節により、胎児細胞とはかなり異なる条件を用いることにより、2週令マウスにおいても同様の培養が可能であることが、DAPIおよびMAP2染色によって確認された。
2.線条体に発現するドーパミン受容体およびベータアドレナリン受容体をそれぞれドーパミン、イソプロテレノールで刺激すると、細胞内cAMP産生は後者による増加量が著名に多かった。しかし、その後の線条体細胞死を測定すると、前者の刺激によって著名に増加することがわかった。
以上の所見から、ドーパミンによる細胞生存の制御メカニズムが推測された。

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Subtype specific cardiac regulation by adenylyl cyclase and its application for the treatment of heart failure by specific ihhibitor

Grant number：16590719 2004 - 2007

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C) Grant-in-Aid for Scientific Research (C)

OKUMURA Satoshi, ISHIKAWA Tfbshihiro, SATO Naoki

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Grant amount：\3840000 （ Direct Cost: \3600000 、 Indirect Cost：\240000 ）

Desensitization of the cAMP signal is a protective mechanism against catecholamine stress on cardiac myocytes to prevent the development of apoptosis. Molecular mechanisms of desensitization have been well studied at the level of receptors, but poorly at the level of the effector enzyme, adenylyl cyclase. To examine the role of type 5 adenylyl cyclase (AC), a major cardiac isoform, in desensitization and apoptosis, we examined the effects of chronic isoproterenol (ISO) infusion in type 5 adenylyl cyclase-null mice (AC5KO) and wild type controls (WT) Desensitization was more effective in AC5KO after infusion, as reflected by a greater degree of downregulation of AC catalytic activity after infusion. WT showed resistance to such desensitization because the type 5 isoform protein expression underwent paradoxical upregulation. The number of apoptotic myocytes was similar at baseline, but significantly smaller in AC5KO after infusion. This was accompanied by a 4-fold greater increase in Bcl-2 and a 3-fold greater increase in phospho-Akt in AC5KO. The latter is most likely through increased membrane localization of PDK1 (phosphoinositide-dependent protein kinase 1), which is known to be inhibited by the CAMP signal. Thus, the property of AC5KO, i.e., enhanced desensitization and protection against apoptosis, suggests that isoform-specific inhibition of type 5 AC may be beneficial following chronic catecholamine stress, and potentially in the treatment of heart failure.

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がん細胞の増殖とカベオリン

Grant number：16022253 2004

日本学術振興会科学研究費助成事業特定領域研究特定領域研究

石川義弘, 南沢享, 戸谷義幸, 岩坪耕策, 堀英明, 常松尚志

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Grant amount：\5900000 （ Direct Cost: \5900000 ）

本研究報告は平成15年からの継続である。カベオリンは分子量20KD程度の、カベオラと呼ばれる細胞膜陥没構造を形成する主要蛋白である。近年カベオリンはカベオラを形成するだけでなく、カベオラに集積する様々な受容体やシグナル蛋白の活性を制御することが知られてきた。カベオリン発現の低下は細胞の増殖を促し、がん細胞において著しく低下していることから、カベオリンは各種増殖シグナルの抑制作用があることがいわれている。我々は昨年度の予備研究結果から、カベオリンが著明ながん細胞の増殖抑制効果を示すことを見出した。そこでこの抑制効果の普遍性を検討するために、さまざまな細胞増殖シグナル受容体作用にたいするカベオリンの効果を検討した。一般的にがん細胞、とりわけ肺がんなどの細胞に対して、カベオリンは増殖抑制にはたらく。しかし、カベオリン3ノックアウト動物を用いた実験から、インシュリンシグナルに関しては例外的に、増強作用があること、同欠損動物はインシュリン抵抗性を示すこと、カベオリン遺伝子の注入によってインシュリン抵抗性の著明な改善が見られることなどがわかった。これらの結果より、カベオリンはインシュリン糖代謝にはむしろ刺激性に働く可能性が示され、カベオリンあるいはその類似蛋白のもつ機能の多様性が示唆された。とりわけ、がん細胞に対する増殖抑制とインシュリンシグナルに対する刺激作用を持ち合わせるカベオリンについては、肝細胞がんの発生との関連が言われるC型肝炎患者における糖尿病の治療等に応用可能であると考えられる。

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Generation of sarcolipin heart-specific transgenic mice and molecular mechanism of atrial chamber-specific expression

Grant number：15500288 2003 - 2004

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C) Grant-in-Aid for Scientific Research (C)

MINAMISAWA Susumu, ISHIKAWA Yoshihiro

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Grant amount：\3600000 （ Direct Cost: \3600000 ）

I. Cardiac dysfunction sarcolipin heart-specific transgenic mice
In vivo echocardiography and hemodynamic study demonstrated that cardiac function, especially diastolic function was impaired in sarcolipin (SLN) heart-specific transgenic mice when compared with those in age-matched control mice. Although SIN heart-specific transgenic mice did not exhibited either cardiac hypertrophy or dilation, molecular markers of cardiac hypertrophy such as ANF and BNP were up regulated, suggesting masked cardiac remodeling in SLN heart-specific transgenic mine. These data indicate that SLN play an important role in atrial function via regulation of SERCA2a activity.
II. Anaiysisi of mouse sarcolipin promoter and its transcriptional regulation
We cloned a 2.3-kilobase pair DNA fragment encompassing the 5'-flanking region of the mouse SLN gene and examined the effect of retinoic acid on its promoter activity. Transient transfection of H9C2 with F1-luciferase (-2237 to +62 nucleotides) yielded a 40-fold increase in promoter activity. Transient transfection of a series of 5'→3' deletion constructs of F1-luciferase suggested that the minimal region for full activation of the SLN promoter activity is located up to -326 nucleotides and that negative regulatory elements of RA were located between -2237 and -326 nucleotides. The present data indicate that the expression of SLN mRNA is likely regulated by retinoic acid, at least in part, at transcriptional level. In addition, we found that pressure overload, retinoic acid and thyroid hormono down-regulated the expression of SLN mRNAs.

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The lack of caveolin-3, muscle-specific subtype of caveolin, leeds to the development of insulin resistance

Grant number：15590951 2003 - 2004

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C) Grant-in-Aid for Scientific Research (C)

TOYA Yoshiyuki, ISHIKAWA Yoshihiro

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Grant amount：\3200000 （ Direct Cost: \3200000 ）

Type 2 diabetes is preceded by the development of insulin resistance, in which the action of insulin is impaired, largely in skeletal muscles. Caveolin-3 is a muscle-specific subtype of caveolin, which is a major component of an example of a scaffolding protein, found within cellular membranes. In this study, we found that the lack of caveolin-3 led to the development of insulin resistance, as exemplified by decrease glucose uptake in skeletal muscles, impaired glucose tolerance test performance, and increases in serum lipids. Such impairments were markedly augmented in the presence of streptozotocin, a pancreatic β cell toxin, suggesting that the mice were susceptible to severe diabetes in the presence of an additional risk factor. Insulin-stimulated activation of receptors and downstream molecules, such as IRS-1 and Akt, was attenuated in the skeletal muscles of caveolin-3 null mice, but not in the liver, without affecting protein expression or sub cellular localization. Genetic transfer of caveolin-3 by needle injection restored insulin signaling in skeletal muscles. Our findings suggest that caveolin-3 is an enhancer of insulin signaling in skeletal muscles but does not act as a scaffolding molecule for insulin receptors. Moreover, We examined the effect of overexpressing caveolin-3 in the liver, which expresses little endogenous caveolin, by adenovirus-mediated gene transfer in diabetic animal models. Gene transfer significantly improved insulin sensitivity in vivo, as shown by an enhanced decline in blood glucose levels upon insulin injection, and thus improved glucose metabolism in diabetic mice, exemplified by greater glucose tolerance test performance and increased glycogen synthesis. Overexpression of caveolin-3 in hepatic cells in vitro led to increased activation of insulin receptors, as well as IRS-1 and Akt, at physiological concentrations of insulin. Our findings suggest that caveolin gene transfer to the liver enhances insulin receptor signal and mimics insulin action.

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The molecular mechanisms for sympathetic regulation of cardiac function

Grant number：15590763 2003 - 2004

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C) Grant-in-Aid for Scientific Research (C)

ISHIKAWA Yoshihiro, MINAMISAWA Susumu, EBINA Toshiaki, TSUNEMATSU Takashi, IWATSUBO Kosaku

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Grant amount：\3300000 （ Direct Cost: \3300000 ）

We have investigated the molecular mechanisms for the regulation of cardiac function by the sympathetic nervous system. For this purpose, we have used newly synthesized P-site inhibitor derivatives and transgenic mouse model in which the expression of type 5 adenylyl cyclase, the major cardiac isoform, is disrupted. We have conducted computer-assisted, drug screening by the use of pharma-core analysis as well as the analysis of the 3D structure of the enzyme protein and miscellaneous compounds. Similarly, we have examined potential changes in cardiac function and the regulation by the sympathetic nervous system in mice with the disrupted type 5 adenylyl cyclase gene.
Most importantly, we have found that by modifying the side chains of classical P-site inhibitors, we can convert them into an adenylyl cyclase isoform-selective inhibitor. In particular, PM6, one of such compounds we have discovered, has demonstrated a high selectivity to the type 5 adenylyl cyclase isoform over other isoforms. Accordingly, the treatment of cardiac myocytes in the presence of this compound significantly attenuated the development of cardiac myocyte apoptosis in response to prolonged catecholamine stimulation. Cardiac myocyte contractility was, however, unaffected, suggesting that this compound can inhibit the development of apoptosis without deteriorating cardiac function. It is thus tentative to speculate that such compound may be useful in the treatment of congestive heart failure, in which beta-adrenergic blockade therapy has been used.
In mice with disrupted type 5 adenylyl cyclase gene, we have found that sympathetic regulation is attenuated on the top of diminished parasympathetic regulation. These findings suggest that type 5 adenylyl cyclase plays a major role in not only regulating sympathetic regulation, but parasympathetic regulation of the heart. We have also examined the effect of chronic catecholamine infusion in adenylyl cyclase-null mice. We have found that the development of cardiac myocyte apoptosis was significantly attenuated in knockout mice as well.

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がん細胞の増殖とカベオリン

Grant number：15024254 2003

日本学術振興会科学研究費助成事業特定領域研究特定領域研究

石川義弘, 戸谷義幸, 南沢享

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Grant amount：\3900000 （ Direct Cost: \3900000 ）

カベオリンは分子量20KD程度の、カベオラと呼ばれる細胞膜陥没構造を形成する主要蛋白である。近年カベオリンはカベオラを形成するだけでなく、カベオラに集積する様々な受容体やシグナル蛋白の活性を制御することが知られてきた。カベオリン発現の低下は細胞の増殖を促し、がん細胞において著しく低下していることから、カベオリンは各種増殖シグナルの抑制作用があることがいわれている。我々はこのカベオリンあるいはフロチリンなどのカベオリン類似分子の機能を、発現調節モデル(細胞培養系および遺伝子操作動物)によって検討する事を目的とした。褐色神経腫細胞において、カベオラ分画に集積する受容体、酵素種を調べたところ、α7型ニコチン受容体の集積が見られたが、他のサブタイプは非カベオラ分画に分布していた。同分画にはアデニル酸シクラーゼ3および6型も集積しており、ニコチン受容体から流入するカルシウムイオンによってアデニル酸シクラーゼ6型の活性制御がなされていることがわかった。また、カベオリン3ノックアウト動物においては筋肉細胞におけるインシュリン糖代謝が低下しており、インシュリン刺激による同受容体のリン酸化の低下および筋肉における糖取り込みの低下が観察された。これらの結果より、カベオリンはインシュリン糖代謝にはむしろ刺激性に働く可能性が示された。以上の結果より、カベオリンあるいはその類似蛋白のもつ機能の多様性が示唆された。

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がん細胞の増殖とカベオリン

Grant number：13216085 2001

日本学術振興会科学研究費助成事業特定領域研究(C) 特定領域研究(C)

石川義弘, 岩本彩雄, 堀英明, 北村均

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Grant amount：\2300000 （ Direct Cost: \2300000 ）

1.ラット筋芽細胞H9C2、心筋組織、血管平滑筋細胞を用いてカベオリン分画の精製を行い、増殖刺激に関与するα1アドレナリン受容体および下流の信号分子の発現分布を検討した。α1受容体、G蛋白質Gq、PLC.βサブタイプ(β1、3)はカベオリン分画に発現が限局していた。さらにα1受容体とカベオリンは免疫沈降実験によって、強く共役していることがわかった。また肥大した心筋細胞でのカベオリン発現を調べ、カベオリン3の発現が有意に肥大心筋において減少していることを見出した。これからカベオリン3の発現低下が、増殖信号の脱抑制を生み、最終的に肥大化をもたらしたと推測された。
2.培養筋原性腫瘍細胞においてカベオリンを誘導性に過大発現させる系を作成し、細胞増殖性と増殖性信号伝達における変化を検討した。カベオリン過大発現によって、カベオリン蛋白は3倍程度に上昇し、形態学的にも細胞膜陥凹構造であるカベオラ数の増大が見られた。カベオリン分画を精製して、発現されたリコンビナントカベオリンの細胞内分布を調べたところ、内因性のものと相違は見られなかった。アンギオテンシン刺激によるERK活性化はカベオリン発現細胞において有意に低下しており、2%FBS刺激存在下で^3Hチミジン取込みを検討した結果、取込み率の有為な減少がみられた。これらの抑制効果はカルシウムキレートやPKC阻害剤によって消失したから、カルシウム感受性PKCサブタイプによる関与が推測された。
3.アデニル酸シクラーゼをサブタイプ選択的に制御する薬物を開発した。各サブタイプをバキュロウイルスシステムにより過大発現させ、フォルスコリン誘導体とコンピュータを用いた立体構造解析から選択された既知の化合物のスクリーニングを行った。この結果、2、3、5サブタイプのそれぞれに選択性を持つ刺激薬を見つけた。さらに5サブタイプを選択的に抑制する新規化合物を発見した。

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SIGNIFICANCE OF THE MULTIPLICITY OF ADENYLYL CYCLASE

Grant number：11480181 1999 - 2000

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B). Grant-in-Aid for Scientific Research (B).

ISHIKAWA Yoshihiro, UMEMURA Satoshi, GOSHIMA Yoshiro, TOYA Yoshiyuki, KITAMURA Hitoshi

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Grant amount：\15800000 （ Direct Cost: \15800000 ）

Recent molecular biological studies have elucidated the presence of multiple adenylyl cyclase isoforms that are different in tissue distribution and biochemical properties. These studies have indicated that the amount and subtype of adenylyl cyclase expressed in each tissue is a key determinant of cAMP signal within the organ. In particular, the heart expresses the two major isoforms of adenylyl cyclase, named type V and VI.We previously demonstrated that these isoforms mostly contribute to the cAMP signal through catecholamine receptors. We have investigated the significance of having multiple adenylyl cyclase isoforms and the distribution of this enzyme within the cell. We have also investigated the biochemical properties of this enzyme using multiple techniques. We have also developed a single step, sucrose gradient centrifugation method that enables easy detection of adenylyl cyclase. Furthermore, we have developed an animal model with deficient adenylyl cyclase type V.During this grant period, we have successfully developed homozygous animals, which will be available to our future studies.

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Regulation of adenylyl cyclase by GTP-binding Proteins

Grant number：07044229 1995 - 1996

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for international Scientific Research Grant-in-Aid for international Scientific Research

KATADA Toshiaki, ISHIKAWA Yoshihiro, HOSHINO Shin-ichi, HAZEKI Osamu

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Grant amount：\7300000 （ Direct Cost: \7300000 ）

GTP-binding protein (G proteins) consisting of alpha, beta, gamma subunits, carry signals from membrane receptors to effectors such as enzymes or ion channels. G proteins dissociate into the GTP-bound alpha and betagamma subunits upon their interaction with agonist-receptor complex. In the present studies, we investigated mechanisms by which the activities of adenylyl cyclase and phosphatidylinositol (PI) 3-kinase are regulated by G proteins, especially the betagamma subunits.
In guinea pig neutrophils, the cellular cAMP formation by prostagladin (PG) E_1 was markedly potentiated by the chemoattractant formyl-Met-Leu-Phe (fMLP). This potentiation was abolished by prior treatment of the cells with pertussis toxin, but not by the prevention of fMLP-induced intracellular Ca^<2+> increase in the cells, indicating the direct involvement of the inhibitory G protein (G_i) in the fMLP-induced potentiation of cAMP formation. Adenylyl cyclase responsible for the G_i-induced potentiation was partially purified from the GTPgammaS-treated cell membranes with a forskolin-agarose column. The cyclase appeared to be a complex form with the GTPgammaS-bound alpha subunit of the stimulatory G_S protein (G_Salpha), but not with the betagamma subunits. The GTPgammaS-bound G_Salpha-stimulated cyclase activity was further enhanced by betagamma subunits. These results indicate that GTP-bound G_Salpha and betagamma subunits released from G_i synergistically stimulate adenylyl cyclase activity in neutrophils. In relation to this, we also found that the activity of PI 3-kinase is inhibited by wortmannin and that several types of PI 3-kinase are stimulated by bg subunits. Interestingly, a peptide containing phosphorylated Tyr and betagamma subunits synergistically activated a certain type of PI 3-kinase. Such synergistic activation was also observed in intact neutrophil-like cells upon their stimulation with insulin and fMLP.Thus, G_i activation appeared to have a cross-talk with Tyr-phosphorylation signaling pathway via betagamma subunits in PI 3-kinase.

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Regulation of ion channels by GTP-binding Proteins

Grant number：05044153 1993 - 1994

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for international Scientific Research Grant-in-Aid for international Scientific Research

KATADA Toshiaki, ISHIKAWA Yoshihiro, KURACHI Yoshihisa, HOSHINO Shin-ichi, HAZEKI Osamu

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Grant amount：\6500000 （ Direct Cost: \6500000 ）

GTP-binding protein (G proteins) consisting of alpha, beta, gamma subunits, carry signals from agonist-bound receptors to effectors such as enzymes or ion channels. Since the functions of G proteins as the signal transducers are profoundly affected by cholera or pertussis toxin which transfers the ADP-ribosyl moiety of NAD^+ to the alpha subunits of G proteins, the toxin-catalyzed ADP-ribosylation has widely been used as a tool to study the roles of G proteins in signal transduction processes. In the present studies, we investigated mechanisms by which the activities of an inwardly rectifying K^+ channel and adenylyl cyclase are regulated by the subunits of G proteins.
1) Activation of inwardly rectifying K^+ channels by the betagamma subunits of G proteins. An inwardly rectifying K^+ channel in guinea pig cardiac atrial cells is activated by the stimulation of muscarinic cholinergic or A^1-purinergic receptors in a manner sensitive to pertussis toxin. In inside-out patches of the cell membranes, the betagamma subunits of G proteins activated the K^+ channels. Properties of the betagamma-induced activation of the K^+ channel appeared to be the same as those observed in GTP-dependent receptor-mediated activation of the K^+ channel. Moreover, the receptor-mediated activation of the K^+ channel was selectively inhibited by GDP-bound from of G_t (transducin). These results indicate that activation of inwardly rectifying K^+ channel coupling to membrane-bound receptors is mediated through the action] of betagammasubunits resolved from alphabetagammatrimer.
2) Activation of adenylyl cyclase by protein kinase C.Cyclic AMP formation within cells is altered upon the activation of protein kinase C.However, the site (s) to be modified by the kinase in the cyclic AMP formation pathway remains unclear. Thus, effects of protein kinase C on the activity of adenylyl cyclase were investigated with purified proteins. Protein kinase C could phosphorylate adenylyl cyclase type V directly, leading to a 20-fold increase in its catalytic activity. This activation was much larger than that stimulated by forskolin (5 fold). When forskolin and the protein phosphorylation were combined, the type 5 cyclase activity was increased more than 100 fold over the basal. Thus, it appears that protein kinase C directly and potently activates adenylyl cyclase.

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第２８回日本病態生理学会大会長

2018.4

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90th Annual Scientific Meeting of Physiological Society of Japan

2013.3

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第９０回日本生理学会大会長

日本生理学会日本生理学会大会

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第２８回日本病態生理学会大会長

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日本病態生理学会日本病態生理学会大会

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NHK総合 2021.7

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NHK総合 2018.7

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Scientific Reports

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Scientific Reports 2015

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Journal of Physiological Sciences

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Journal of Physiological Sciences 2013 - 2019

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Pharmacological Reviews

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Pharmacological Reviews 2011 - 2020

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Cardiovascular Research

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Cardiovascular Research 2008

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Journal of Sleep Disorders and Therapy

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Journal of Sleep Disorders and Therapy 2012 - 2014

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2011 - 2019

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Current Signal Transduction Therapy

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Current Signal Transduction Therapy 2009

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Journal of Bioanalysis and Biomedicine 2009

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Open Medicinal Chemistry 2009 - 2011

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日本循環器学会専門医 2008 - 2009

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Journal of Cardiovascular Pharmacology 2003

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