Elucidation of molecular mechanism of mechanotransduction in the heart

2016 Fiscal Year Final Research Report

• Project/Area Number: 26282122
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Biomedical engineering/Biomaterial science and engineering
• 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.

Free Research Field

医工学、生理学、細胞生理学、生化学、形態学