2016 Fiscal Year Final Research Report
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 |
Section | 一般 |
Research Field |
Biomedical engineering/Biomaterial science and engineering
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Research Institution | Okayama University |
Principal Investigator |
Katanosaka Yuki 岡山大学, 医歯(薬)学総合研究科, 助教 (60432639)
|
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)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
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 |
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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Free Research Field |
医工学、生理学、細胞生理学、生化学、形態学
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