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- W2912477877 abstract "Introduction and aimsCalcific aortic valve disease (CAVD) is the most common heart valve disease in western countries. It has been reported that activation of the calcium-sensing receptor(CaSR) expressed by vascular smooth muscle cells prevents vascular calcification. However, to date, the CaSR's expression and function in cardiac valves have not been studied. The present study sought to evaluate the presence of the CaSR within human valvular interstitial cells (hVICs), assess the CaSR's functionality, and ascertain its involvement in hVIC calcification.Methods and resultsData from Western blot, flow cytometry and immunocytochemistry experiments demonstrated that primary hVICs express the CaSR. The receptor was functional, since the incubation of hVICs with the calcimimetic R-568 significantly increased Ca2+-induced ERK1/2 phosphorylation, and exposure to the calcilytic NPS2143 reduced ERK1/2 activation. A reduction in endogenous CaSR expression by hVICs (using siRNA) was associated with significantly lower levels of Ca2+-induced mineralization (quantified using Alizarin Red staining). Similar data were obtained after the pharmacological inhibition of CaSR activity by the calcilytic NPS2143. In contrast, overexpression of a functional CaSR amplified Ca2+-induced calcification. Pharmacological activation of the CaSR with the calcimimetic R-568 showed similar effects. CaSR's procalcific properties are associated with increased osteogenic transition (as characterized by elevated mRNA expression of bone morphogenetic protein 2 and osterix), and reduced the expression of the calcification inhibitor osteopontin. Histological analysis of 12 human aortic tricuspid valves showed that CaSR expression was greater in calcified areas than in non-calcified areas. These data were confirmed by Western blots.ConclusionsTo the best of our knowledge, this study is the first to have demonstrated that hVICs express a functional CaSR. Taken as a whole, our data suggest that activation of the CaSR expressed by hVICs might be a key promoter of CAVD progression." @default.
- W2912477877 created "2019-02-21" @default.
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- W2912477877 date "2019-04-01" @default.
- W2912477877 modified "2023-09-27" @default.
- W2912477877 title "Activation of the calcium-sensing receptor in human valvular interstitial cells promotes calcification" @default.
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- W2912477877 cites W1967483573 @default.
- W2912477877 cites W1967487729 @default.
- W2912477877 cites W1972065681 @default.
- W2912477877 cites W1983925075 @default.
- W2912477877 cites W1985945376 @default.
- W2912477877 cites W1986677563 @default.
- W2912477877 cites W199420291 @default.
- W2912477877 cites W1996750235 @default.
- W2912477877 cites W2006851263 @default.
- W2912477877 cites W2009441758 @default.
- W2912477877 cites W2012669950 @default.
- W2912477877 cites W2013004133 @default.
- W2912477877 cites W2017579147 @default.
- W2912477877 cites W2041595300 @default.
- W2912477877 cites W2053975726 @default.
- W2912477877 cites W2059245505 @default.
- W2912477877 cites W2074760181 @default.
- W2912477877 cites W2077900736 @default.
- W2912477877 cites W2080632245 @default.
- W2912477877 cites W2084388540 @default.
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- W2912477877 cites W2109064733 @default.
- W2912477877 cites W2115813002 @default.
- W2912477877 cites W2122367477 @default.
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- W2912477877 cites W2135663788 @default.
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- W2912477877 cites W2140233920 @default.
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- W2912477877 doi "https://doi.org/10.1016/j.yjmcc.2019.01.021" @default.
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