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miR-19b attenuates H2O2-induced apoptosis in rat H9C2 cardiomyocytes via targeting PTEN
Jiahong Xu1, Yu Tang1, Yihua Bei2
1Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China.
Abstract:
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.
Insights
Myocardial ischemia-reperfusion (I-R) injury treatment is limited. This study reveals miR-19b protects heart cells by reducing apoptosis, suggesting miR-19b therapy for I-R injury.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Cellular Stress Response
Background:
- Myocardial ischemia-reperfusion (I-R) injury presents significant therapeutic challenges.
- The miR-17-92 microRNA cluster is implicated in cell proliferation and apoptosis, but its role in I-R injury is unclear.
Purpose of the Study:
- To investigate the role of the miR-17-92 cluster, specifically miR-19b, in myocardial I-R injury.
- To determine the therapeutic potential of modulating miR-19b in the context of I-R injury.
Main Methods:
- Utilized a murine model of myocardial I-R injury and H2O2-treated H9C2 cardiomyocytes to mimic oxidative stress.
- Employed flow cytometry and Western blot analysis to assess apoptosis, cell survival, and protein expression.
- Investigated the regulatory relationship between miR-19b and its downstream target, PTEN.
Main Results:
- miR-19b was significantly downregulated in the infarct area of I-R injured hearts and in H2O2-treated cardiomyocytes.
- Overexpression of miR-19b reduced apoptosis and enhanced cell survival under oxidative stress.
- PTEN was identified as a direct downstream target of miR-19b, mediating its protective effects against apoptosis.
Conclusions:
- miR-19b plays a protective role in mitigating myocardial I-R injury by inhibiting apoptosis.
- PTEN is a key mediator in the miR-19b pathway during oxidative stress in cardiomyocytes.
- miR-19b represents a potential novel therapeutic target for treating myocardial I-R injury.
