| Project/Area Number |
21790101
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Biological pharmacy
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| Research Institution | Mukogawa Women's University |
|---|
Principal Investigator |
NAKASE Tomoka Mukogawa Women's University, 薬学部, 講師 (40434807)
|
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| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 細胞死 / オートファジー / アポトーシス / 心筋 / 虚血 / 心筋細胞 / グルコース |
|---|
| Research Abstract |
Non-apoptotic cell death in ischemic heart disease is considered to be one of the important therapeutic targets, however, the detailed mechanisms of this cell death process is not clear. In this study, we found that hypoxic myocyte death was independent of caspases and involved with calcium-independent phospholipase A_2 (iPLA_2). The potent cardioprotective corticotropin-releasing hormone (CRH), urocortin and peptide hormone leptin suppress caspase-independent, non-apoptotic death in myocytes exposed to ischemia. On the other hand, autophagy prevents ischemic injury dependent on glucose concentration and is required for cardioprotective activity of 17-β-estradiol.
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