Research Papers: Pathology:
miR-19b attenuates H2O2-induced apoptosis in rat H9C2 cardiomyocytes via targeting PTEN
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Jiahong Xu1,*, Yu Tang1,*, Yihua Bei2,*, Shengguang Ding3, Lin Che1, Jianhua Yao4, Hongbao Wang4, Dongchao Lv2 and Junjie Xiao2
1 Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China
2 Regeneration and Ageing Laboratory, Experimental Center of Life Sciences, School of Life Science, Shanghai University, Shanghai, China
3 Department of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of NanTong University, Nantong, China
4 Department of Cardiology, Shanghai Yangpu District Hospital, Tongji University School of Medicine, Shanghai, China
* These authors have contributed equally to this work
Junjie Xiao, email:
Dongchao Lv, email:
Keywords: ischemia reperfusion injury, cardiomyocytes, apoptosis, microRNA, PTEN, Pathology Section
Received: August 30, 2015 Accepted: February 15, 2016 Published: February 24, 2016
Myocardial ischemia-reperfusion (I-R) injury lacks effective treatments. The miR-17-92 cluster plays important roles in regulating proliferation, apoptosis, cell cycle and other pivotal processes. However, their roles in myocardial I-R injury are largely unknown. In this study, we found that miR-19b was the only member of the miR-17-92 cluster that was downregulated in infarct area of heart samples from a murine model of I-R injury. Meanwhile, downregulation of miR-19b was also detected in H2O2-treated H9C2 cells in vitro mimicking oxidative stress occurring during myocardial I-R injury. Using flow cytometry and Western blot analysis, we found that overexpression of miR-19b decreased H2O2-induced apoptosis and improved cell survival, while downregulation of that had inverse effects. Furthermore, PTEN was negatively regulated by miR-19b at the protein level while silencing PTEN could completely block the aggravated impact of miR-19b inhibitor on H2O2-induced apoptosis in H9C2 cardiomyocytes, indicating PTEN as a downstream target of miR-19b controlling H2O2-induced apoptosis. These data indicate that miR-19b overexpression might be a novel therapy for myocardial I-R injury.
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