| Project/Area Number |
26462336
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Anesthesiology
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
KOJIMA Akiko 滋賀医科大学, 医学部, 助教 (50447877)
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| Co-Investigator(Kenkyū-buntansha) |
北川 裕利 滋賀医科大学, 医学部, 教授 (50252391)
松浦 博 滋賀医科大学, 医学部, 教授 (60238962)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 心筋保護効果 / 心筋虚血再灌流傷害 / Ca2+輸送タンパク質 / TRPCチャネル / 心筋リアノジン受容体 / 麻酔学 / 心保護効果 / 吸入麻酔薬 / Ca2+制御タンパク質 / 細胞内Ca2+過負荷 / 虚血再灌流傷害 / RyR2 / SOCE |
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| Outline of Final Research Achievements |
Intracellular Ca2+ overload during ischemia/reperfusion in myocardium is responsible for cellular injury leading to cardiac dysfunction, namely ischemia/reperfusion injury. Because various Ca2+ transport proteins, such as type 2 ryanodine receptor (RyR2) and store-operated Ca2+ entry (SOCE) channel, are involved in Ca2+ overload-induced cellular injury, we investigated whether blocking these channels is effective in reducing the cardiac ischemia/reperfusion injury.
In mouse hearts subjected to ischemia/reperfusion, contractile functions of left ventricle were significantly reduced compared with these baseline value. In contrast, administration of RyR2 blocker or SOCE channel blockers ameliorated the contractile dysfunction after ischemia/reperfusion. These results indicate that RyR2 and SOCE channel are involved in the development of cardiac ischemia/reperfusion injury and can provide the potential therapeutic targets to prevent the heart from ischemia/reperfusion injury.
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