| Project/Area Number |
15H06182
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Legal medicine
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
Noritake Kanako 東京医科歯科大学, 大学院医歯学総合研究科, 特任助教 (40758067)
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| Project Period (FY) |
2015-08-28 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | エタノール / 心筋細胞傷害 / Hippo-YAP経路 / 細胞間接着 / 心筋障害 / 細胞間接着分子 |
|---|
| Outline of Final Research Achievements |
Excessive alcohol consumption often causes compromised myocardial contractile function, although the precise mechanism remains unknown. We reported previously that when mouse atrium-derived HL-1 cardiomyocytes undergo apoptosis upon direct exposure to ethanol, the cellular cytoskeleton is severely disrupted and the anti-apoptotic transcriptional co-activator YAP is inactivated. The restoration of YAP activation rescues the cells from apoptosis: both the expression of constitutively active YAP and the stabilization of the actomyosin cytoskeleton prevent ethanol-induced cell death. Thus, a decrease in actin tension and YAP inactivation should be crucially involved in the cytotoxicity of ethanol on HL-1 cardiomyocytes.
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