| Project/Area Number |
25460287
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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 |
General physiology
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KOJIMA Akiko 滋賀医科大学, 医学部, 助教 (50447877)
TOYODA Futoshi 滋賀医科大学, 医学部, 助教 (90324574)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 虚血再灌流傷害 / 容量性カルシウム流入機構 / Ca2+過負荷 / 筋小胞体 / リアノジン受容体 / 2-APB / フレカイニド / ランゲンドルフ灌漑 / 心肥大モデルマウス / TAC手術 / 心室筋細胞 / Ca2+/カルモジュリン依存性タンパクキナーゼ / 筋小胞体リアンジン受容体 / カルシウムリーク / C57BL/6Jマウス / 大動脈狭窄 / 細胞拘縮 / 筋小胞体リアノジン受容体 / RyR2 / 容量性（ストア調節性）Ca2+流入機構 / SOCE / マウス摘出灌流心 / 左心室機能 / LaCl3 / TRPC |
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| Outline of Final Research Achievements |
The present investigation provides experimental evidence to support that the store-operated Ca2+ entry (SOCE) is involved in ischemia/reperfusion injury in the heart. For example, in Langendorff-perfused mouse heart model, reperfusion following 30 min of global ischemia was associated with contractile dysfunction such as elevation of left ventricular end-diastolic pressure and reduction of left ventricular developed pressure. These dysfunctions were partially but significantly attenuated by the SOCE blockers 2-aminoethoxydiphenyl borate (2-APB) and LaCl3. In addition, flecainide, which blocks Ca2+ leak through type2 ryanodine receptor and thereby preserves Ca+ content in SR, was also effective in preventing the contractile dysfunction associated with ischemia/reperfusion injury in the heart. These observations suggest that the drugs that block Ca2+ leak from SR have protective effects against ischemia/reperfusion injury in the heart.
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