Publication date: April 2018
Source:Biomedicine & Pharmacotherapy, Volume 100
Author(s): Ruixia Qiu, Wen Li, Yunhai Liu
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.
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Medicine by Alexandros G. Sfakianakis,Anapafseos 5 Agios Nikolaos 72100 Crete Greece,00302841026182,00306932607174,alsfakia@gmail.com,
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Τρίτη 6 Φεβρουαρίου 2018
MicroRNA-204 protects H9C2 cells against hypoxia/reoxygenation-induced injury through regulating SIRT1-mediated autophagy
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