| Project/Area Number |
24790788
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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 |
Circulatory organs internal 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 | 生体分子 / シグナル伝達 / 分子心臓病態学 / サイトカイン / IL17 |
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| Research Abstract |
Post-infarct mortality was prevented in interleukin-17 knockout mice (IL17-KO) compared with wild-type mice. Left ventricular dysfunction, increase in LV weight to body weight ratio, and myocardial fibrosis 28 days after myocardial infarction were significantly attenuated in IL17-KO mice compared with wild-type mice. To investigate the mechanism for left ventricular remodeling inhibition in IL17-KO mice, we conducted microarray analysis. Microarray analysis revealed that the expressions of extracellular matrix related genes were lower in IL17-KO mice than those in wild-type mice. These results suggest that IL17 may play a pathogenic role in the development of left ventricular remodeling after myocardial infarction, possibly through the regulation of extracellular matrix genes expression.
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