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MiR-93 inhibition ameliorates OGD/R induced cardiomyocyte apoptosis by targeting Nrf2
1Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. qcg123@163.com.
Objective:
To identify the expression changes of microRNA 93 (miR-93) in oxygen-glucose deprivation/reoxygenation (OGD/R) injury in cardiomyocytes and its mechanism of mediating OGD/R and inducing apoptosis.
Materials And Methods:
Primary cardiomyocytes were extracted and OGD/R model in cardiomyocytes was established in vitro. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expressions of miR-93, and Western blot assay was applied to measure the protein levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and caspase-3. Flow cytometry was utilized to examine the cardiomyocyte apoptosis rate.
Results:
The apoptosis rate was increased after OGD/R in cardiomyocytes, accompanied by remarkable rise of miR-93 expression. After transfection of miR-93 antagomir, the apoptosis rate of cardiomyocyte induced by OGD/R was down-regulated, and the expression of cleaved caspase-3 was decreased. Meanwhile, the results of qRT-PCR and Western blot showed that the levels of Nrf2 mRNA and protein expression were up-regulated after the miR-93 level was inhibited, and luciferase reporter assay affirmed that Nrf2 was a target molecule for OGD/R-induced apoptosis mediated by miR-93.
Conclusions:
miR-93 mediates OGD/R-induced hypoxia/reoxygenation injury apoptosis in cells by targeting Nrf2.
Insights
MicroRNA 93 (miR-93) expression increases during oxygen-glucose deprivation/reoxygenation (OGD/R) injury in cardiomyocytes. Inhibiting miR-93 reduces apoptosis by targeting Nrf2, offering a potential therapeutic strategy.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Cellular Stress Response
Background:
- Oxygen-glucose deprivation/reoxygenation (OGD/R) is a key factor in myocardial ischemia-reperfusion injury.
- Understanding the molecular mechanisms of OGD/R-induced cardiomyocyte apoptosis is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of microRNA 93 (miR-93) in OGD/R-induced cardiomyocyte injury.
- To elucidate the mechanism by which miR-93 mediates apoptosis during OGD/R.
Main Methods:
- Establishment of an in vitro OGD/R model using primary cardiomyocytes.
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) to measure miR-93 expression.
- Western blot to assess nuclear factor erythroid 2-related factor 2 (Nrf2) and caspase-3 protein levels.
- Flow cytometry to quantify cardiomyocyte apoptosis.
Main Results:
- OGD/R significantly increased cardiomyocyte apoptosis and miR-93 expression.
- Inhibition of miR-93 using an antagomir reduced OGD/R-induced apoptosis and cleaved caspase-3 levels.
- miR-93 inhibition led to increased Nrf2 mRNA and protein expression.
- Luciferase reporter assays confirmed Nrf2 as a direct target of miR-93.
Conclusions:
- miR-93 plays a critical role in mediating apoptosis in cardiomyocytes subjected to OGD/R.
- The miR-93/Nrf2 pathway is a key mechanism underlying OGD/R-induced cardiac injury.
- Targeting miR-93 may represent a novel therapeutic approach for myocardial ischemia-reperfusion injury.
