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Published on: June 15, 2018
MicroRNA-210 alleviates oxidative stress-associated cardiomyocyte apoptosis by regulating BNIP3
Hongying Diao1, Bin Liu1, Yongfeng Shi1
1a Department of Cardiology , The Second Hospital of Jilin University , Changchun , People's Republic of China.
Abstract:
Oxidative stress-induced myocardial apoptosis and necrosis are involved in ischemia/reperfusion (I/R) injury. This study was performed to investigate microRNA (miR)-210's role in oxidative stress-related myocardial damage. The expression of miR-210 was upregulated in myocardial tissues of I/R rats, while that of Bcl-2 adenovirus E1B 19kDa-interacting protein 3 (BNIP3) was downregulated. To simulate in vivo oxidative stress, H9c2 cells were treated with H2O2 for 48 h. MiR-210 level was increased upon H2O2 stimulation, peaked at 8 h, and then decreased. An opposite expression pattern of BNIP3 was observed. BNIP3 was demonstrated as a direct target of miR-210 via luciferase reporter assay. H2O2-induced cell apoptosis was attenuated by miR-210 mimics, whereas aggravated by miR-210 inhibitor. MiR-210 knockdown-induced cell apoptosis in presence of H2O2 was attenuated by BNIP3 siRNA. Our work demonstrates that miR-210 plays a protective role in H2O2-induced cardiomyocyte apoptosis at least by regulating the pro-apoptotic BNIP3.
Insights
MicroRNA-210 protects heart cells from oxidative stress by regulating BNIP3. This finding is crucial for understanding and treating ischemia/reperfusion injury and myocardial damage.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Cellular Stress Response
Background:
- Ischemia/reperfusion (I/R) injury involves oxidative stress, leading to myocardial apoptosis and necrosis.
- MicroRNAs (miRNAs) are key regulators of cellular processes, including stress responses.
Purpose of the Study:
- To investigate the role of microRNA-210 (miR-210) in oxidative stress-induced myocardial damage.
- To elucidate the relationship between miR-210 and Bcl-2 adenovirus E1B 19kDa-interacting protein 3 (BNIP3) in cardiomyocytes.
Main Methods:
- Assessed miR-210 and BNIP3 expression in an in vivo rat model of I/R injury.
- Utilized H9c2 cells treated with hydrogen peroxide (H2O2) to simulate oxidative stress.
- Performed luciferase reporter assays to confirm BNIP3 as a direct target of miR-210.
- Employed miR-210 mimics/inhibitors and BNIP3 siRNA to evaluate effects on apoptosis.
Main Results:
- miR-210 expression was upregulated in I/R rat myocardial tissues, while BNIP3 was downregulated.
- H2O2 treatment increased miR-210 and decreased BNIP3 in H9c2 cells.
- miR-210 mimics reduced H2O2-induced apoptosis, whereas miR-210 inhibitors aggravated it.
- BNIP3 knockdown attenuated apoptosis in H2O2-treated cells with miR-210 knockdown.
Conclusions:
- miR-210 plays a protective role against oxidative stress-induced cardiomyocyte apoptosis.
- This protective effect is mediated, at least in part, by the regulation of the pro-apoptotic protein BNIP3.
- Findings highlight miR-210 as a potential therapeutic target for myocardial I/R injury.
