Oncotarget

Research Papers: Pathology:

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

Zun-Ping Ke, Peng Xu, Yan Shi and Ai-Mei Gao _

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Oncotarget. 2016; 7:28796-28805. https://doi.org/10.18632/oncotarget.8941

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Abstract

Zun-Ping Ke1,*, Peng Xu1,*, Yan Shi2 and Ai-Mei Gao3

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.


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