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10.1080/15384101.2019.1580494 http://scihub22266oqcxt.onion/10.1080/15384101.2019.1580494 C6464590!6464590 !30810438     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30810438 &cmd=llinks): Failed to open stream: HTTP request failed! 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Overexpression of microRNA-202-3p protects against myocardial ischemia-reperfusion injury through activation of TGF-?1/Smads signaling pathway by targeting TRPM6 |pdf=|usr=}}{{30810438 }} gab.com Text Overexpression of microRNA-202-3p protects against myocardial ischemia-reperfusion injury through activation of TGF- 1/Smads signaling pathway by targeting TRPM6 JO: Cell Cycle http://www.kidney.de/pget.php?&tw=1&pmid=30810438 #FOAvip MicroRNAs (miRNAs) have been found to act as key regulators in the pathogenesis of myocardial ischemic-reperfusion (I/R) injury. In this study, we explore the role and mechanism of microRNA-202-3p (miR-202-3p) in regulating cardiomyocyte apoptosis, in respective of the TGF-?1/Smads signaling pathway by targeting the transient receptor potential cation channel, subfamily M, member 6 (TRPM6). The targeting relationship between miR-202-3p and TRPM6 was verified by a dual-luciferase reporter gene assay. Sprague-Dawley rat models of myocardial I/R injury were initially established and treated with different mimics, inhibitors and siRNAs to test the effects of miR-202-3p and TRPM6 on myocardial I/R injury. The levels of inflammatory factors; IL-1?, IL-6, TNF-? as well as the degree of myocardial fibrosis and cardiomyocyte apoptosis were determined in rats transfected with different plasmids. TRPM6 was found to be the target of miR-202-3p. Up-regulated miR-202-3p or knockdown of TRPM-6 alleviated oxidative stress and inflammatory response, reduced ventricular mass, altered cardiac hemodynamics, suppressed myocardial infarction, attenuated cell apoptosis, and inhibited myocardial fibrosis. MiR-202-3p overexpression activates the TGF-?1/Smads signaling pathway by negatively regulating TRPM6 expression. Taken together, these findings suggest that miR-202-3p offers protection against ventricular remodeling after myocardial I/R injury via activation of the TGF-?1/Smads signaling pathway. Twit Text FOAVip Overexpression of microRNA-202-3p protects against myocardial ischemia-reperfusion injury through activation of TGF- 1/Smads signaling pathway by targeting TRPM6 ????Cell Cycle http://www.kidney.de/pget.php?&tw=1&pmid=30810438 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30810438 #FOAvip English Wikipedia <ref>{{Cite pmid|30810438 }}</ref> Overexpression of microRNA-202-3p protects against myocardial ischemia-reperfusion injury through activation of TGF-?1/Smads signaling pathway by targeting TRPM6 #MMPMID30810438 Wu HY ; Wu JL ; Ni ZL Cell Cycle 2019[Mar]; 18 (5 ): 621-637 PMID30810438 show ga MicroRNAs (miRNAs) have been found to act as key regulators in the pathogenesis of myocardial ischemic-reperfusion (I/R) injury. In this study, we explore the role and mechanism of microRNA-202-3p (miR-202-3p) in regulating cardiomyocyte apoptosis, in respective of the TGF-?1/Smads signaling pathway by targeting the transient receptor potential cation channel, subfamily M, member 6 (TRPM6). The targeting relationship between miR-202-3p and TRPM6 was verified by a dual-luciferase reporter gene assay. Sprague-Dawley rat models of myocardial I/R injury were initially established and treated with different mimics, inhibitors and siRNAs to test the effects of miR-202-3p and TRPM6 on myocardial I/R injury. The levels of inflammatory factors; IL-1?, IL-6, TNF-? as well as the degree of myocardial fibrosis and cardiomyocyte apoptosis were determined in rats transfected with different plasmids. TRPM6 was found to be the target of miR-202-3p. Up-regulated miR-202-3p or knockdown of TRPM-6 alleviated oxidative stress and inflammatory response, reduced ventricular mass, altered cardiac hemodynamics, suppressed myocardial infarction, attenuated cell apoptosis, and inhibited myocardial fibrosis. MiR-202-3p overexpression activates the TGF-?1/Smads signaling pathway by negatively regulating TRPM6 expression. Taken together, these findings suggest that miR-202-3p offers protection against ventricular remodeling after myocardial I/R injury via activation of the TGF-?1/Smads signaling pathway. |Animals [MESH] |Antagomirs/metabolism [MESH] |Apoptosis [MESH] |Cytokines/metabolism [MESH] |Disease Models, Animal [MESH] |Male [MESH] |MicroRNAs/antagonists & inhibitors/genetics/*metabolism [MESH] |Myocardial Reperfusion Injury/metabolism/*pathology [MESH] |Oxidative Stress [MESH] |RNA Interference [MESH] |RNA, Small Interfering/metabolism [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Signal Transduction [MESH] |Smad Proteins/*metabolism [MESH] |Superoxide Dismutase/metabolism [MESH] |TRPM Cation Channels/antagonists & inhibitors/genetics/*metabolism [MESH] |Transforming Growth Factor beta1/*metabolism [MESH]Overexpression of microRNA-202-3p protects against myocardial ischem(epmc).pdf DeepDyve Pubget Overpricing