2016 Fiscal Year Final Research Report
Analysis of dilated cardiomyopathy phenotyoe in cardiac-specific SOCS3 deficient mice.
| Project/Area Number |
26461137
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Kurume University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | 心不全 / 拡張型心筋症 / 心筋細胞 / SOCS3 / JAK-STAT / オートファジー |
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| Outline of Final Research Achievements |
Suppressor of cytokine signaling-3 (SOCS3) is a cytokine-inducible negative regulator of JAK-STAT signaling pathway. Cardiac-specific SOCS3 deficient mice (SOCS3-CKO) spontaneously develop cardiac dysfunction with advanced age. In this study, we analysed the underlying mechanism of age-related cardiac dysfunction in SOCS3-cKO mice. We found that developed cardiac dysfunction estimated by echocardiogram and increased activation of STAT3 from 25 weeks of age in SOCS3-CKO. In SOCS3-CKO mice hearts from 25 weeks of age, LC3II/LC3I ratio was significantly decreased. Western blot analysis revealed that expression of parkin and PINK1 but not p62 and Bnip3 were decreased in SOCS3-CKO mice compared with control mice from 25 weeks of age. These results suggest that age-related cardiac dysfunction in SOCS3-CKO mice may be due to impaired autophagy through sustained STAT3 activation.
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| Free Research Field |
分子心臓学
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