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MicroRNA-137 Negatively Regulates H₂O₂-Induced Cardiomyocyte Apoptosis Through CDC42
Junnan Wang1, Rihao Xu1, Junduo Wu1
1Department of Cardiovascular Surgery, The Second Hospital of Jilin University, Changchun, Jilin, China (mainland).
Background:
Oxidative stress, inducing cardiomyocyte apoptosis or myocardial ischemia, is the major denominator of many cardiac diseases. In this study, we intended to explore the regulatory function of microRNA-137 (miR-137) in oxidative stress-induced cardiomyocyte apoptosis.
Material And Methods:
Cardiomyocytes were extracted from newborn C57BL/6 mice and cultured in vitro. Apoptosis was induced by H2O2, and evaluated by TUNEL assay. The effect of cardiomyocyte apoptosis on gene expression of miR-137 was evaluated by qRT-PCR. Lentivirus was used to stably down-regulate miR-137, and the subsequent effects of miR-137 down-regulation on cardiomyocyte apoptosis, its targeted gene CDC42, and caspase pathway were evaluated by TUNEL assay, dual-luciferase reporter assay, and Western blot assay, respectively. Finally, CDC42 was down-regulated by siRNA and its effect on miR-137-mediated cardiomyocyte apoptosis protection was examined.
Results:
H2O2 induced significant apoptosis and up-regulated miR-137 in cardiomyocytes, whereas lentivirus-mediated miR-137 down-regulation protected against apoptosis. CDC42 was the direct target gene of miR-137 and proteins of CDC42, caspase-3, and caspase-9 were all regulated by miR-137 down-regulation in cardiomyocyte apoptosis. SiRNA-mediated CDC42 down-regulation reversed the protection of miR-137 down-regulation against cardiomyocyte apoptosis.
Conclusions:
Our work demonstrated miR-137 and CDC42 are critical regulators in cardiomyocyte apoptosis. It may help to identify the molecular targets to prevent myocardial injury in human patients.
Insights
MicroRNA-137 (miR-137) protects against oxidative stress-induced cardiomyocyte apoptosis by targeting CDC42. Down-regulating miR-137 or CDC42 impacts cardiac cell survival, offering potential therapeutic targets for myocardial injury.
Area of Science:
- Cardiology
- Molecular Biology
- Cell Biology
Background:
- Oxidative stress is a key factor in cardiac diseases, leading to cardiomyocyte apoptosis and myocardial ischemia.
- Understanding the role of microRNAs in regulating these processes is crucial for developing new treatments.
Purpose of the Study:
- To investigate the regulatory role of microRNA-137 (miR-137) in oxidative stress-induced cardiomyocyte apoptosis.
- To identify the molecular targets and pathways involved in miR-137's function.
Main Methods:
- Cardiomyocytes were subjected to hydrogen peroxide (H2O2) to induce apoptosis.
- miR-137 levels were modulated using lentivirus, and its effects on apoptosis, target gene CDC42, and caspase pathways were assessed.
- Western blot and dual-luciferase reporter assays were employed to validate targets and protein expression.
Main Results:
- H2O2 induced significant cardiomyocyte apoptosis and upregulated miR-137 expression.
- Down-regulation of miR-137 protected cardiomyocytes from apoptosis and affected CDC42, caspase-3, and caspase-9 protein levels.
- CDC42 was identified as a direct target of miR-137, and its down-regulation reversed the protective effects of miR-137 modulation.
Conclusions:
- miR-137 and CDC42 are critical regulators of cardiomyocyte apoptosis.
- These findings suggest potential molecular targets for preventing myocardial injury in patients.
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