2017 Fiscal Year Final Research Report
Selenoprotein P, a liver-derived secretory protein, regulates pressure overload-induced cardiac remodeling
| Project/Area Number |
15K09135
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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 | Kanazawa University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | 心臓リモデリング / 心不全 / 心肝連関 / ヘパトカイン |
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| Outline of Final Research Achievements |
Selenoprotein P (SeP) is a liver-derived secretory protein that impairs insulin signal transduction and induces insulin resistance and hyperglycemia. Although clinical studies suggest the insulin resistance is an independent risk factor of heart failure, the role of SeP in pathogenesis of chronic heart failure is not well understood. We investigated the role of SeP in the regulation of cardiac remodeling in response to pressure overload. Transverse aortic constriction (TAC) was subjected to SeP knockout (KO) and wild-type (WT) mice for 2 weeks. The mortality rate following TAC was significantly decreased in SeP KO mice compared to WT mice. LV weight/body weight (BW) and Lung weight/BW were significantly smaller in SeP KO mice than in WT mice. Furthermore, mRNA expression of collagen 1a1 significantly less in SeP KO compared to WT. These results suggest that the absence of endogenous SeP attenuated cardiac hypertrophy, dysfunction and fibrosis in response to pressure overload in mice
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| Free Research Field |
循環器内科
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