MicroRNA-93 inhibits ischemia-reperfusion induced cardiomyocyte apoptosis by targeting PTEN

// Zun-Ping Ke 1,* , Peng Xu 1,* , Yan Shi 2 and Ai-Mei Gao 3 1 Department of Cardiology, The Fifth People’s Hospital of Shanghai, Fudan University, Shanghai, China 2 Department of Emergency, The Affiliated Huai’an Hospital of Xuzhou Medical College and The Second People’s Hospital of Huai’an, Huai’an, China 3 Department of Pharmacy, The Fifth People’s Hospital of Shanghai, Fudan University, Shanghai, China * These authors have contributed equally to this study and share first authorship Correspondence to: Ai-Mei Gao, email: // Keywords : microRNA-93, ischemia/reperfusion, PTEN, AKT, apoptosis, Pathology Section Received : January 19, 2016 Accepted : April 04, 2016 Published : April 22, 2016 Abstract MicroRNAs have been implicated in some biological and pathological processes, including the myocardial ischemia/reperfusion (I/R) injury. Recent findings demonstrated that miR-93 might provide a potential cardioprotective effect on ischemic heart disease. This study was to investigate the role of miR-93 in I/R-induced cardiomyocyte injury and the potential mechanism. In this study, we found that hypoxia/reoxygenation (H/R) dramatically increased LDH release, MDA contents, ROS generation, and endoplasmic reticulum stress (ERS)-mediated cardiomyocyte apoptosis, which were attenuated by co-transfection with miR-93 mimic. Phosphatase and tensin homolog (PTEN) was identified as the target gene of miR-93. Furthermore, miR-93 mimic significantly increased p-Akt levels under H/R, which was partially released by LY294002. In addtion, Ad-miR-93 also attenuated myocardial I/R injury in vivo , manifested by reduced LDH and CK levels, infarct area and cell apoptosis. Taken together, our findings indicates that miR-93 could protect against I/R-induced cardiomyocyte apoptosis by inhibiting PI3K/AKT/PTEN signaling.