Related Experiment Video
Updated: Mar 8, 2026

In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
Published on: June 15, 2018
MicroRNA-135a Regulates Apoptosis Induced by Hydrogen Peroxide in Rat Cardiomyoblast Cells
Ning Liu1, Yong-Feng Shi1, Hong-Ying Diao1
1Department of Cardiology, The Second Hospital of Jilin University, Changchun, Jilin, 130041, China.
Abstract:
Oxidative stress and apoptosis are the most important pathologic features of ischemic heart disease. Recent research has indicated that microRNAs (miRs) play an essential role in apoptosis. However, whether miRs might regulate B cell lymphoma-2 (Bcl-2) protein in apoptosis during ischemic heart disease is still unclear. The aim of this study, therefore, was to confirm the regulation of microRNA-135a (miR-135a) in oxidative stress injuries induced by hydrogen peroxide (H2O2) in rat cardiomyoblast cells H9c2. To this end, we analyzed the effects of H2O2 treatment on miR-135a expression in rat cardiomyocytes. Furthermore, we upregulated and inhibited miR-135a using mimics and inhibitors, respectively, and examined the effects on cell viability and apoptosis-related proteins. We observed that miR-135a was markedly up-regulated under H2O2 treatment in rat cardiomyoblast cells. Overexpression of miR-135a blocked the Bcl-2 protein and enhanced the apoptosis induced by H2O2, and miR-135a inhibition restored Bcl-2 protein expression. Interestingly, miR-135a inhibition did not attenuate H2O2-induced apoptosis with Bcl-2 knockdown. The results of the present study indicate that miR-135a regulates H2O2-induced apoptosis in H9c2 cells via targeting Bcl-2, and that miR-135a may be a novel therapeutic target for ischemic heart disease.
Insights
MicroRNA-135a (miR-135a) targets Bcl-2 protein, increasing apoptosis in oxidative stress. Inhibiting miR-135a may offer a new therapeutic strategy for ischemic heart disease.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Cell Biology
Background:
- Ischemic heart disease involves oxidative stress and apoptosis.
- MicroRNAs (miRs) are implicated in apoptosis regulation.
- The role of miRs in regulating Bcl-2 during ischemic heart disease is not fully understood.
Purpose of the Study:
- To investigate the role of microRNA-135a (miR-135a) in oxidative stress-induced apoptosis in rat cardiomyoblast cells (H9c2).
- To determine if miR-135a regulates the expression of Bcl-2 protein in this context.
- To explore miR-135a as a potential therapeutic target for ischemic heart disease.
Main Methods:
- H9c2 cells were treated with hydrogen peroxide (H2O2) to induce oxidative stress.
- miR-135a expression levels were analyzed.
- miR-135a was upregulated using mimics and inhibited using inhibitors.
- Cell viability and apoptosis-related proteins, including Bcl-2, were assessed.
Main Results:
- H2O2 treatment significantly upregulated miR-135a expression in H9c2 cells.
- Overexpression of miR-135a reduced Bcl-2 protein levels and enhanced H2O2-induced apoptosis.
- Inhibition of miR-135a restored Bcl-2 expression.
- Bcl-2 knockdown abolished the anti-apoptotic effect of miR-135a inhibition.
Conclusions:
- miR-135a directly targets Bcl-2, mediating apoptosis in H2O2-induced oxidative stress in H9c2 cells.
- miR-135a plays a critical role in the apoptotic pathway during oxidative stress.
- miR-135a represents a potential novel therapeutic target for managing ischemic heart disease.
Related Concept Videos
The Intrinsic Apoptotic Pathway
MicroRNAs
Peroxisomes

