| Project/Area Number |
16590534
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Legal medicine
|
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| Research Institution | The University of Tokyo |
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Principal Investigator |
UEMURA Koichi The University of Tokyo, Graduate School of Medicine, Lecturer, 大学院・医学系研究科, 講師 (30244586)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIDA Ken-ichi The University of Tokyo, Graduate School of Medicine, Professor, 大学院・医学系研究科, 教授 (40166947)
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| Project Period (FY) |
2004 – 2005
|
| Project Status |
Completed (Fiscal Year 2005)
|
| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2005: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2004: ¥2,800,000 (Direct Cost: ¥2,800,000)
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| Keywords | carbon monoxide / ischemia / reactive oxygen species / necrosis / apoptosis / calcium / H9c2 / L-type Ca^<2+> channel / 細胞死 |
|---|
| Research Abstract |
Carbon monoxide (CO) is known to protect myocardial and vascular cells against injuries due to ischemia-reperfusion or inflammation. We showed that a C^<2+>-dependent protease calpain promotes necrotic cell death of cardiomyocyte-derived H9c2 cells due to hypoxia through α-fodrin proteolysis. Here, we show that ischemia induces necrotic cell death, which is inhibited by either CO, extracellular Ca^<2+> deprivation or L-type Ca^<2+> channel blockers. A whole cell patch clamp experiments supports that CO inhibits L-type Ca^<2+> channel mediated influx of Ca^<2+> and the ischemic death of H9c2 cells.
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