Journal of Shanghai University(Natural Science Edition) ›› 2019, Vol. 25 ›› Issue (1): 10-17.doi: 10.12066/j.issn.1007-2861.2097

• Precision and Translational Medicine • Previous Articles     Next Articles

Role of miR-19b in protecting cardiomyocytes from apoptosis by activating Akt signaling

ZHU Hongwen1, YU Pujiao2, XU Jiahong2()   

  1. 1. Department of Cardiology, Anting Hospital,Shanghai 201805, China
    2. Department of Cardiology, Tongji Hospital Affiliated to Tongji University, Shanghai 200065, China
  • Received:2018-10-26 Online:2019-02-28 Published:2019-02-26
  • Contact: XU Jiahong E-mail:xujiahong@tongji.edu.cn

Abstract:

[Objective] The purpose of the research is to investigate the effects of miR-19b on apoptosis and its underlying mechanisms in the oxygen glucose deprivation/reperfusion (OGD/R) model of neonatal rat cardiomyocytes (NRCMs). [Methods] NRCMs are obtained from neonatal rats by enzymatic hydrolysis and then transfected by miR-19b mimics and miR-19b inhibitor for the following study. A model of OGD/R has been built in NRCMs to mimic myocardial ischemia and reperfusion injury (MIRI). Terminal deoxynucleotidyl transferase (TdT)-mediated 2'-deoxyuridine 5'-triphosphate (dUTP)-biotion nick end labeling (TUNEL) assay has been performed to detect cardiomyocyte apoptosis. Western blot has been applied for detecting the expression of apoptotic proteins (Bcl2, Bax and Caspase3) and the downstream proteins of miR-19b. TUNEL staining indicates that miR-19b mimics could reduce the ratio of TUNEL positive nucleus to total nucleus and miR-19b inhibitor has opposite effects. [Results] Results based on western blot support the observations above. Moreover, miR-19b mimics could down-regulate the expression of phosphatase and tensin homolog (PTEN) and activate Akt signaling while miR-19b inhibitor has opposite effects. The rescue experiment has confirmed that PTEN-siRNA could reverse the promotion of miR-19b inhibitor on cardiomyocyte apoptosis. [Conclusion] miR-19b may protect cardiomyocytes from apoptosis through the activation of Akt signaling via regulating PTEN negatively.

Key words: cardiomyocytes apoptosis, miR-19b, Akt signaling

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