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Updated: May 4, 2026
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
MicroRNA-22 targeting CBP protects against myocardial ischemia-reperfusion injury through anti-apoptosis in rats
Jian Yang1, Lihua Chen, Jun Yang
1Department of Cardiology, The First College of Clinical Medical Sciences, China Three Gorges University, Yichang, 443000, Hubei, China.
Abstract:
MicroRNAs are extensively involved in the pathogenesis of major cardiovascular diseases by suppressing target gene expression. Recent studies have reported that microRNA-22 (miR-22) may be implicated in ischemia-reperfusion (I/R) induced myocardial injury. However, the specific function of miR-22 in myocardial I/R injury is far from clear nowadays. The present study was designed to determine the role of miR-22 in myocardial I/R injury and investigate the underlying cardio-protective mechanism. The rat myocardial I/R injury model was induced by occluding the left anterior descending coronary artery for 30 min followed by 12 h reperfusion. As predicted, adenovirus-mediated miR-22 overexpression markedly reduced the release of creatine kinase and lactate dehydrogenase, infarct size and cardiomyocytes apoptosis. Moreover, CREB binding protein (CBP) as a potential miR-22 target by bioinformatics was significantly inhibited after miR-22 transfection. We also found that p53 acetylation activity, pro-apoptotic related genes Bax and p21 levels were all decreased associated with the down-regulation of CBP. In conclusion, our data demonstrate that miR-22 could inhibit apoptosis of cardiomyocytes through one of its targets, CBP. Thus, miR-22 may constitute a new therapeutic target for the prevention of myocardial I/R injury.
Insights
MicroRNA-22 (miR-22) protects the heart from injury after ischemia-reperfusion (I/R). Overexpressing miR-22 reduces heart cell death and damage by inhibiting CREB binding protein (CBP), offering a potential therapeutic target.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Gene Regulation
Background:
- MicroRNAs regulate gene expression and are implicated in cardiovascular diseases.
- MicroRNA-22 (miR-22) is suggested to play a role in myocardial ischemia-reperfusion (I/R) injury, but its precise function remains unclear.
Purpose of the Study:
- To elucidate the role of miR-22 in myocardial I/R injury.
- To investigate the cardioprotective mechanisms mediated by miR-22.
Main Methods:
- Established a rat model of myocardial I/R injury.
- Utilized adenovirus-mediated miR-22 overexpression.
- Assessed cardiac injury markers, infarct size, and cardiomyocyte apoptosis.
- Investigated the interaction between miR-22 and CREB binding protein (CBP) using bioinformatics and experimental validation.
Main Results:
- Overexpression of miR-22 significantly reduced creatine kinase and lactate dehydrogenase release, infarct size, and cardiomyocyte apoptosis.
- Bioinformatic analysis identified CREB binding protein (CBP) as a target of miR-22.
- miR-22 transfection inhibited CBP expression, leading to decreased p53 acetylation activity and reduced levels of pro-apoptotic genes Bax and p21.
Conclusions:
- miR-22 exerts a cardioprotective effect against myocardial I/R injury by inhibiting cardiomyocyte apoptosis.
- This protective mechanism involves the downregulation of CBP, a key target of miR-22.
- miR-22 represents a promising therapeutic target for preventing myocardial I/R injury.
