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发布于:2020-12-25 12:37:26  访问:44 次 回复:0 篇
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Re reported to be connected with hypertrophic cardiomyopathy and coronary artery
Canonical transient receptor protein 1 (TRPC1) encoded by the TRPC1 gene is an ion U18666A site channel situated on the plasma membrane of many human and animal cell types23. TRPC1 is believed to mediate calcium entry in response to depletion of endoplasmic calcium stores or activation of receptors coupled for the phospholipase C system24. Functionally, TRPC1 is involved in cardiac hypertrophy, hypertension, vascular inflammation and cancer25,26. Having said that, alterations of these genes in SFI- treated hypertrophic cardiomyocytes have not been studied prior to. In our study, the protein expressions of MEF2A, -MHC, BNP and TRPC1 have been drastically enhanced after PE treatment, which proved to become a state beneath hypertrophic conditions. Our information suggest that MEF2A is aSCientifiC REPORTS | (2018) eight:4660 | DOI:ten.1038s41598-018-23137-www.nature.comscientificreportstarget of miR-19a-3p, and A 1120 MedChemExpress miR-19a-3p up-regulation could minimize the expression of MEF2A mRNA and protein. In addition, lower-expression of miR-19a-3p may possibly improve the expression of MEF2A, -MHC, BNP and TRPC1 in cardiomyocyte hypertrophy, which seemingly implies that lower-expression of miR-19a-3p mediated MEF2 signaling may be a trigger of myocardial hypertrophy. Interestingly, SFI could reverse these situations. Usually, our study adds new clues for the understanding about the action mechanism of SFI in the therapy of myocardial hypertrophy. We suppose that dysregulation and function of miR-19a-3p within the myocardium play a crucial function in myocardial hypertrophy. Over-expression of miR-19a-3p inside the myocardium might prove to be capable to attenuate myocardial hypertrophy. MEF2A is inhibited by miR-19a-3p below physiological circumstances, and through the myocardial hypertrophy procedure also. These final results also imply that miR-19a-3p may perhaps regulate MEF2-related genes. Our study suggested that SFI attenuated myocardial hypertrophy possibly by enhancing the expression of miR-19a-3p and down-regulating the expression of MEF2A, -MHC, BNP and TRPC1, which seemingly implies that the SFI mediated improvement within MEF2 signaling might be the result in of attenuated myocardial hypertrophy. It is worth noting that, according to the miRNA microarray information, it seems that the advantage of SFI is because of upregulation and downregulation of a number of miRNAs. SFI is often a conventional Chinese medicine preparation, and its function in cardiac hypertrophy seems to become multi-targeting. In our existing study, the regulation of miR-19a-3p expression only represents one action of SFI‘s targets. Furthermore, viral-mediated overexpression of miR-19a-3p in the rat hypertrophy mod.Re reported to be associated with hypertrophic cardiomyopathy and coronary artery disease179. MEF2A, which has been shown in Knock-out studies, is essential for energy metabolism and sarcomeric organisation in adult hearts15. The MEF2 family members can also be viewed as an essential transcription aspect in myocyte hypertrophy and is involved in mediating the hypertrophic action of glucose on cardiomyocytes20, however the regulatory relationship with MEF2 and miRNA is much less clear. Interestingly, our study showed that MEF2A was the target gene of miR-19a-3p, and it was highly expressed inside the hypertrophic myocardium model under lower-expression of miR-19a-3p. TRP channels are a loved ones of non-selective cation channels that function as polymodal sensors in different physiological and pathological processes21,22.
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