| Project/Area Number |
24791957
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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 |
Emergency medicine
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| Research Institution | Kurume University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | アポトーシス / シグナル / 救急医学 / 集中治療医学 |
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| Research Abstract |
We investigated the role of myocardial suppressor of cytokine signaling-3 (SOCS3), an intrinsic negative feedback regulator of the JAK-STAT signaling pathway, in the pathophysiology of myocardial ischemia-reperfusion(I/R) injury. Activation of cardioprotective signaling pathways including STAT3, AKT, and ERK1/2 were rapidly peaked and was inactivated after I/R. Although the initial infarct size after coronary occlusion determined by triphenyltetrazolium chloride staining was comparable between control and cardiac-specific SOCS3 knockout mice (SOCS3-CKO), the infarct size 24 h after I/R was reduced by approximately 30% in SOCS3-CKO mice, indicating that progression of myocardial I/R injury was prevented in SOCS3-CKO hearts. Cardiac-specific SOCS3 deletion enhanced multiple cardioprotective signaling pathways including STAT3, AKT and ERK1/2 while inhibiting myocardial apoptosis.
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