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

Zun-Ping Ke, Peng Xu, Yan Shi, Ai-Mei Gao
Author Information
  1. Zun-Ping Ke: Department of Cardiology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
  2. Peng Xu: Department of Cardiology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
  3. Yan Shi: Department of Emergency, The Affiliated Huai'an Hospital of Xuzhou Medical College and The Second People's Hospital of Huai'an, Huai'an, China.
  4. Ai-Mei Gao: Department of Pharmacy, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.

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.

Keywords

References

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MeSH Term

Animals
Apoptosis
Humans
MicroRNAs
Myocardial Reperfusion Injury
Myocytes, Cardiac
PTEN Phosphohydrolase
Rats
Rats, Sprague-Dawley

Chemicals

MIRN93 microRNA, human
MicroRNAs
PTEN Phosphohydrolase

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