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Updated: Jan 5, 2026
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
MiR-183-5p protects rat hearts against myocardial ischemia/reperfusion injury through targeting VDAC1
Duomao Lin1, Boqun Cui1, Jun Ma1
1Center for Anesthesiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Abstract:
MicroRNAs have been reported to be implicated in myocardial ischemia/reperfusion (I/R) injury. The purpose of this study was to investigate the effect of miR-183-5p on I/R injury. Overexpression of miR-183-5p by agomiR transfection alleviated cardiac dysfunction and significantly reduced the infarct size in rats with myocardial I/R. MiR-183-5p also alleviated myocardial apoptosis with reduced apoptotic cells and lower levels of apoptosis associated proteins. in vitro experiments were conducted on rat H9c2 cells treated with anoxia/reoxygenation (A/R). Annexin V/propidium iodide (PI) staining and flow cytometry reported that the ratio of apoptotic cells decreased by miR-183-5p transfection before A/R treatment. Moreover, according to binding sequence prediction and Dual luciferase reporter assay, we explored that voltage-dependent anion channel 1 (VDAC1), which aggravates myocardial injury and apoptosis reported in our former research, was a target of miR-183-5p. In conclusion, miR-183-5p can efficiently attenuate I/R injury and miR-183-5p may exert its effect through repressing VDAC1 expression.
Insights
MicroRNA-183-5p (miR-183-5p) overexpression protects against myocardial ischemia/reperfusion (I/R) injury by reducing cardiac dysfunction and apoptosis. It achieves this by targeting and repressing voltage-dependent anion channel 1 (VDAC1) expression.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- MicroRNA Therapeutics
Background:
- Myocardial ischemia/reperfusion (I/R) injury is a significant clinical challenge.
- MicroRNAs (miRNAs) are increasingly recognized for their roles in cardiac pathophysiology.
- The specific role of miR-183-5p in I/R injury requires further elucidation.
Purpose of the Study:
- To investigate the therapeutic potential of miR-183-5p in myocardial I/R injury.
- To elucidate the underlying molecular mechanisms of miR-183-5p action in cardiac I/R.
Main Methods:
- In vivo studies using a rat model of myocardial I/R with agomiR-mediated miR-183-5p overexpression.
- In vitro studies using rat H9c2 cells subjected to anoxia/reoxygenation (A/R).
- Assessment of cardiac function, infarct size, apoptosis markers, and VDAC1 expression.
- Bioinformatic prediction and Dual luciferase reporter assays to identify miRNA targets.
Main Results:
- Overexpression of miR-183-5p significantly reduced infarct size and improved cardiac function in rats with I/R injury.
- miR-183-5p transfection decreased myocardial apoptosis and levels of apoptosis-associated proteins.
- In vitro, miR-183-5p transfection reduced A/R-induced apoptosis in H9c2 cells.
- VDAC1 was identified as a direct target of miR-183-5p.
Conclusions:
- miR-183-5p effectively attenuates myocardial I/R injury.
- miR-183-5p exerts its protective effects, at least in part, by repressing VDAC1 expression.
- miR-183-5p represents a potential therapeutic target for managing I/R injury.
