Elucidation of molecular mechanism of mechanotransduction in the heart
| Project/Area Number |
26282122
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Biomedical engineering/Biomaterial science and engineering
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| Research Institution | Okayama University |
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Principal Investigator |
Katanosaka Yuki 岡山大学, 医歯(薬)学総合研究科, 助教 (60432639)
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| Co-Investigator(Kenkyū-buntansha) |
毛利 聡 川崎医科大学, 医学部, 教授 (00294413)
金川 基 神戸大学, 医学(系)研究科(研究院), 講師 (00448044)
片野坂 公明 中部大学, 公私立大学の部局等, 准教授 (50335006)
中村 一文 岡山大学, 医歯(薬)学総合研究科, 准教授 (10335630)
氏原 嘉洋 川崎医科大学, 医学部, 助教 (80610021)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥16,510,000 (Direct Cost: ¥12,700,000、Indirect Cost: ¥3,810,000)
Fiscal Year 2016: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2014: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
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| Keywords | メカノセンサー / 心筋細胞 / リモデリング / カルシウム / チャネル / 血行動態負荷 / 心肥大 / 心不全 / 心臓 / 循環器・高血圧 / 生理学 / タンパク質 / 遺伝子 / トランスレーショナルリサーチ / メカニカルストレス / 血行動態 / 高血圧 / 分子生理 |
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| Outline of Final Research Achievements |
The heart has a dynamic compensatory mechanism for haemodynamic stress. However, the molecular details of myocardial mechanotransduction have remained unclear. Here we generated temporally-controlled cardiac-specific transient receptor potential, vanilloid family type 2 (TRPV2)-deficient mice. The elimination of cardiac TRPV2 resulted in a rapid and severe decline in cardiac function, with abnormal cellular morphology, intracellular Ca2+ handling, and contractility. These results suggested that TRPV2 is critical for the maintenance of cardiac structure and function.
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Report
(4 results)
Research Products
(30 results)
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[Journal Article] TRPV2 is critical for the maintenance of cardiac structure and function in mice.2014
Author(s)
Katanosaka Y, Iwasaki K, Ujihara Y, Takatsu S, Nishitsuji K, Kanagawa M, Sudo A, Toda T, Katanosaka K, Mohri S, Naruse K.
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Journal Title
Nat Comm
Volume: 5
Issue: 1
Pages: 3932-3932
DOI
NAID
Related Report
Peer Reviewed / Open Access
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[Journal Article] Overexpression of LARGE suppresses muscle regeneration via down-regulation of insulin like growth factor 1 and aggravates muscular dystrophy in mice.2014
Author(s)
Saito F, Kanagawa M, Ikeda M, Hagiwara H, Masaki T, Ohkuma H, Katanosaka Y, Shimizu T, Sonno M, Toda T, Matsumura K.
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Journal Title
Hum Mol Genet.
Volume: 23
Pages: 4543-4558
Related Report
Peer Reviewed / Open Access
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[Journal Article] Involvement of S1P1 receptor pathway in angiogeniceffects of a novel adenosine-like nucleic acid analog COA-Cl in cultured human vascular endothelial cells.2014
Author(s)
Junsuke Igarashi, Takeshi Hashimoto, Yasuo Kubota, Kazuyo Shoji, Tokumi Maruyama, Norikazu Sakakibara, Yoh Takuwa, Yoshihiro Ujihara, Yuki Katanosaka, Satoshi Mohri, Keiji Naruse, Tetsuo Yamashita, Ryuji Okamoto, Katsuya Hirano, Hiroaki Kosaka, Maki Takata,Ryoji Konishi, Ikuko Tsukamoto.
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Journal Title
Pharmacology Research and Perspectives
Volume: -
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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