| Literature DB >> 29421577 |
Ruixia Qiu1, Wen Li2, Yunhai Liu3.
Abstract
Ischemia/reperfusion (I/R) injury is a main cause of acute myocardial infarction, and the pathogenesis of I/R injury is still not definitely confirmed. In the present study, we aimed to explore the roles of miR-204 in hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury in vitro. The H9C2 cells were subjected to hypoxia for 12 h followed by reoxygenation for another 24 h, and we found that miR-204 was significantly down-regulated after H/R treatment. Transfection of miR-204 mimics attenuated the H/R-induced impaired cell viability and increased apoptosis rates. Furthermore, SIRT1 was identified as a direct target of miR-204, and its expression is negatively regulated by miR-204. Forced expression of SIRT1 could partly rescue the effects of miR-204 on H/R-induced apoptosis and autophagy. Taken together, our study first revealed that overexpression of miR-204 has a protective effect against myocardial I/R injury.Entities:
Keywords: Apoptosis; Autophagy; H9C2 cells; Hypoxia/reoxygenation injury; SIRT1; microRNA-204
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Year: 2018 PMID: 29421577 DOI: 10.1016/j.biopha.2018.01.165
Source DB: PubMed Journal: Biomed Pharmacother ISSN: 0753-3322 Impact factor: 6.529