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10.1038/s41598-017-02585-4 http://scihub22266oqcxt.onion/10.1038/s41598-017-02585-4 C5443797!5443797!28539652     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28539652&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2017 ; 7 (ä): ä Nephropedia Template TP {{tp|p=28539652|t=2017. ANO1 inhibits cardiac fibrosis after myocardial infraction via TGF-?/smad3 pathway |pdf=|usr=}}{{28539652}} gab.com Text ANO1 inhibits cardiac fibrosis after myocardial infraction via TGF- /smad3 pathway JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28539652 #FOAvip As a newly identified factor in calcium-activated chloride channel, ANO1 participates in various physiological processes like proliferation and differentiation, and expresses in human cardiac fibroblasts. In this experiment, we investigated the function of ANO1 in cardiac fibrosis after myocardial infraction (MI) with methods of Western blotting, Quantitative real-time PCR (qRT-PCR), metabolic reduction of 3-(4,5-dimethylthiozol-2-yl)-2, 5-diphenyltetrazo-lium bromide (MTT), immunofluorescence and confocal imaging, and Masson?s trichrome staining. The results showed that the expression of ANO1 significantly increased in neonatal rats? cardiac fibroblasts after hypoxia and in cardiac tissues after MI. After ANO1 over-expression, cardiac fibrosis was reduced in vitro and in vivo. Moreover, the expression of TGF-? and p-smad3 declined after ANO1over-expression in cardiac fiborblasts. In conclusion, ANO1 inhibits cardiac fibrosis after MI via TGF-?/smad3 pathway in rats. Twit Text FOAVip ANO1 inhibits cardiac fibrosis after myocardial infraction via TGF- /smad3 pathway ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28539652 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28539652 #FOAvip English Wikipedia <ref>{{Cite pmid|28539652}}</ref> ANO1 inhibits cardiac fibrosis after myocardial infraction via TGF-?/smad3 pathway #MMPMID28539652 Gao Y; Zhang YM; Qian LJ; Chu M; Hong J; Xu D Sci Rep 2017[]; 7 (ä): ä PMID28539652show ga As a newly identified factor in calcium-activated chloride channel, ANO1 participates in various physiological processes like proliferation and differentiation, and expresses in human cardiac fibroblasts. In this experiment, we investigated the function of ANO1 in cardiac fibrosis after myocardial infraction (MI) with methods of Western blotting, Quantitative real-time PCR (qRT-PCR), metabolic reduction of 3-(4,5-dimethylthiozol-2-yl)-2, 5-diphenyltetrazo-lium bromide (MTT), immunofluorescence and confocal imaging, and Masson?s trichrome staining. The results showed that the expression of ANO1 significantly increased in neonatal rats? cardiac fibroblasts after hypoxia and in cardiac tissues after MI. After ANO1 over-expression, cardiac fibrosis was reduced in vitro and in vivo. Moreover, the expression of TGF-? and p-smad3 declined after ANO1over-expression in cardiac fiborblasts. In conclusion, ANO1 inhibits cardiac fibrosis after MI via TGF-?/smad3 pathway in rats. äANO1 inhibits cardiac fibrosis after myocardial infraction via TGF-?/s(epmc).pdf DeepDyve Pubget Overpricing