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Trimetazidine protects against hypoxia-reperfusion-induced cardiomyocyte apoptosis by increasing microRNA-21 expression |pdf=|usr=}}{{26097555 }} gab.com Text Trimetazidine protects against hypoxia-reperfusion-induced cardiomyocyte apoptosis by increasing microRNA-21 expression JO: Int J Clin Exp Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26097555 #FOAvip Myocardial tissue injury caused by ischemia and hypoxia is a major cause of fatal diseases, including coronary atherosclerosis resulting from myocardial infarction and stroke. Trimetazidine (TMZ), as an anti-ischemic and antioxidant agent, has been demonstrated to preventing ischemia/reperfusion-induced cardiomyocyte apoptosis. However, the anti-apoptosis mechanism of TMZ has not been fully elucidated. The present study demonstrated that miR-21 involved trimetazidine-induced anti-apoptosis during H/R injury in H9C2 cell. In this study, TMZ increased miR-21 expression which further upregulated the Akt signaling activity via suppressing the expression of phosphatase and tensin homolog (PTEN) in H/R H9C2 cell. The increased activity of Akt signaling decreased the ratio of Bax/Bcl-2 and the expression of caspase-3 and inhibited H/R induced apoptosis. In conclusion, this study revealed the mechanism that TMZ up-regulated miR-21 expression, then miR-21 targeted PTEN increasing the PI3K pathway and finally the activation of this pathway counteracted the apoptotic effect of hypoxia/reperfusion. Twit Text FOAVip Trimetazidine protects against hypoxia-reperfusion-induced cardiomyocyte apoptosis by increasing microRNA-21 expression ????Int J Clin Exp Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26097555 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26097555 #FOAvip English Wikipedia <ref>{{Cite pmid|26097555 }}</ref> Trimetazidine protects against hypoxia-reperfusion-induced cardiomyocyte apoptosis by increasing microRNA-21 expression #MMPMID26097555 Yang Q ; Yang K ; Li AY Int J Clin Exp Pathol 2015[]; 8 (4 ): 3735-41 PMID26097555 show ga Myocardial tissue injury caused by ischemia and hypoxia is a major cause of fatal diseases, including coronary atherosclerosis resulting from myocardial infarction and stroke. Trimetazidine (TMZ), as an anti-ischemic and antioxidant agent, has been demonstrated to preventing ischemia/reperfusion-induced cardiomyocyte apoptosis. However, the anti-apoptosis mechanism of TMZ has not been fully elucidated. The present study demonstrated that miR-21 involved trimetazidine-induced anti-apoptosis during H/R injury in H9C2 cell. In this study, TMZ increased miR-21 expression which further upregulated the Akt signaling activity via suppressing the expression of phosphatase and tensin homolog (PTEN) in H/R H9C2 cell. The increased activity of Akt signaling decreased the ratio of Bax/Bcl-2 and the expression of caspase-3 and inhibited H/R induced apoptosis. In conclusion, this study revealed the mechanism that TMZ up-regulated miR-21 expression, then miR-21 targeted PTEN increasing the PI3K pathway and finally the activation of this pathway counteracted the apoptotic effect of hypoxia/reperfusion. |Apoptosis/*drug effects [MESH] |Caspase 3/metabolism [MESH] |Cell Line [MESH] |Humans [MESH] |Hypoxia/metabolism [MESH] |MicroRNAs/*metabolism [MESH] |Myocardial Reperfusion Injury/*metabolism [MESH] |Myocytes, Cardiac/*drug effects/metabolism [MESH] |PTEN Phosphohydrolase/metabolism [MESH] |Proto-Oncogene Proteins c-akt/metabolism [MESH] |Signal Transduction/physiology [MESH] |Trimetazidine/*pharmacology [MESH]Trimetazidine protects against hypoxia-reperfusion-induced cardiomyocy(epmc).pdf DeepDyve Pubget Overpricing