| Project/Area Number |
25860622
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Keio University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 途絶心筋 / 心筋プレコンディショニング / 虚血再灌流障害 / ストレス応答ホルモン / 小胞体ストレス / 遺伝子改変マウス / ミトコンドリア障害 / 酸化ストレス / eif2α / 虚血再灌流傷害 |
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| Outline of Final Research Achievements |
A change of cardiac function after ischemic-perfusion injury has two types; myocardial stunning (transient cardiac dysfunction) and ischemic preconditioning (tolerance to ischemia). We hypothesized that eukaryotic translation initiation factor2α (eIF2α) was related to myocardial stunning and ischemic preconditioning. First of all, we made genetically modified mice whose elF2α in hearts could be controlled at arbitrary level. When eIF2α was moderately activated, the mice hearts showed tolerance to ischemic-perfusion injury. And when eIF2α was highly activated, transient cardiac dysfunction emerged. Then we demonstrated the relationship between eIF2α and ischemic-reperfusion injury with genomic, metabolomic, calcium dynamic analysis and electron microscopes.
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