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10.3892/mmr.2017.6397 http://scihub22266oqcxt.onion/10.3892/mmr.2017.6397 C5428907!5428907!28350072     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Med+Rep 2017 ; 15 (5): 3041-7 Nephropedia Template TP {{tp|p=28350072|t=2017. The role of miR-370 in fibrosis after myocardial infarction |pdf=|usr=}}{{28350072}} gab.com Text The role of miR-370 in fibrosis after myocardial infarction JO: Mol Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=28350072 #FOAvip In the present study, we investigated the expression of miR-370 in the border area of infarction after myocardial infarction and its role in the process of post-infarction fibrosis. A myocardial infarction model in Sprague-Dawley rats was established. After two weeks, the mRNA levels of transforming growth factor-?1 (TGF?1), TGF?RII, ColIa1, ColIIIa1 and miR-370 and the expression of TGF?1, TGF?RII and ?-smooth muscle actin (?-SMA) proteins in the border area of infarction were detected by real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) and western blot analysis. Cardiac fibroblasts in neonatal rat were isolated and cultured, and the changes in the above indicators were detected after AngII and miR-370 intervention. Luciferase reporter gene assay was conducted to verify whether TGF?RII was a target gene of miR-370. In the border area after myocardial infarction, the expression of miR-370 decreased, while mRNA levels of TGF?1, TGF?RII, ColIa1 and ColIIIa1 and levels of TGF?1, TGF?RII and ?-SMA proteins were all increased. Luciferase reporter gene assay confirmed that TGF?RII was the target gene of miR-370. miR-370 reduced the expression of TGF?RII and inhibited the increased expression of TGF?RII and collagen protein caused by AngII. As well, its inhibited the differentiation effect of muscle fibroblasts while it did not inhibit the expression of TGF?1. miR-370 inhibited the expression of TGF?RII protein by combining with TGF?RII mRNA. miR-370 also partially blocked TGF?1-TGF?RII and induced the downstream signal transduction pathways, thus exerting anti-fibrotic effects. Twit Text FOAVip The role of miR-370 in fibrosis after myocardial infarction ????Mol Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=28350072 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28350072 #FOAvip English Wikipedia <ref>{{Cite pmid|28350072}}</ref> The role of miR-370 in fibrosis after myocardial infarction #MMPMID28350072 Yuan H; Gao J Mol Med Rep 2017[May]; 15 (5): 3041-7 PMID28350072show ga In the present study, we investigated the expression of miR-370 in the border area of infarction after myocardial infarction and its role in the process of post-infarction fibrosis. A myocardial infarction model in Sprague-Dawley rats was established. After two weeks, the mRNA levels of transforming growth factor-?1 (TGF?1), TGF?RII, ColIa1, ColIIIa1 and miR-370 and the expression of TGF?1, TGF?RII and ?-smooth muscle actin (?-SMA) proteins in the border area of infarction were detected by real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) and western blot analysis. Cardiac fibroblasts in neonatal rat were isolated and cultured, and the changes in the above indicators were detected after AngII and miR-370 intervention. Luciferase reporter gene assay was conducted to verify whether TGF?RII was a target gene of miR-370. In the border area after myocardial infarction, the expression of miR-370 decreased, while mRNA levels of TGF?1, TGF?RII, ColIa1 and ColIIIa1 and levels of TGF?1, TGF?RII and ?-SMA proteins were all increased. Luciferase reporter gene assay confirmed that TGF?RII was the target gene of miR-370. miR-370 reduced the expression of TGF?RII and inhibited the increased expression of TGF?RII and collagen protein caused by AngII. As well, its inhibited the differentiation effect of muscle fibroblasts while it did not inhibit the expression of TGF?1. miR-370 inhibited the expression of TGF?RII protein by combining with TGF?RII mRNA. miR-370 also partially blocked TGF?1-TGF?RII and induced the downstream signal transduction pathways, thus exerting anti-fibrotic effects. äThe role of miR-370 in fibrosis after myocardial infarction (epmc).pdf DeepDyve Pubget Overpricing