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Updated: Jan 26, 2026

Acute Myocardial Infarction in Rats
Published on: February 16, 2011
MiR-34a regulates cell apoptosis after myocardial infarction in rats through the Wnt/β-catenin signaling pathway
1Department of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China. wch1201@126.com.
Objective:
To explore the molecular mechanism of micro ribonucleic acid-34a (miR-34a) in promoting the apoptosis of myocardial cells in the rat model of myocardial infarction (MI).
Materials And Methods:
Sprague-Dawley (SD) rats were ligated with a left anterior descending branch to construct the MI model. The rats were randomly divided into four groups: sham operation group (Sham group), MI group, MI + miR-34a inhibitor group (MI + miR-34a antagomir group) and MI + miR-34a inhibitor negative control group (MI + antagomir NC group). Echocardiography (ECG) and magnetic resonance imaging (MRI) were adopted to detect the ejection fraction [EF (%)] and fraction shortening [FS (%)] of SD rats. Polymerase chain reaction (PCR) and Western blotting were used to detect expression levels of the apoptotic marker Caspase-3 and genes in Wnt/β-catenin signaling pathway. Hematoxylin and eosin (H&E) staining was applied to detect cardiac injury. In in vitro experiments, the rat-derived myocardial cell line H9C2 was selected to simulate myocardial ischemia and hypoxia at the time of MI with an anoxic and serum-free injury model. C59, the Wnt/β-catenin signaling pathway inhibitor was applied in MI + miR-34a antagomir + C59 group, and the effect of miR-34a on the apoptosis of myocardial cells through regulating the Wnt/β-catenin pathway was measured with Real-Time quantitative PCR (qPCR) and 3-(4,5)-dimethylthiazol(-z-y1)-3,5-diphenyltetrazolium bromide (MTT) cell activity detection kits, respectively.
Results:
It was found that after miR-34a antagomir reversed FS (%) and EF (%) in MI rats, the messenger RNA (mRNA) and protein levels of Caspase-3 in Sham group and MI + miR-34a antagomir group were significantly lower than those in the MI group (p < 0.05), indicating that the addition of miR-34a antagomir inhibited myocardial cell apoptosis after infarction, while the mRNA and protein levels of Wnt/β-catenin were both higher than those in the MI group. Besides, H&E staining proved that miR-34a reversed the myocardial injury after MI. Similarly, in vitro experiments showed that, compared with those in Hypoxia group, the level of Caspase-3 decreased in Hypoxia + miR-34a inhibitor group and Sham group, while the apoptosis level in Hypoxia + miR-34a inhibitor + C59 group increased (p < 0.05). The results of the MTT assay were consistent with those of PCR. MiR-34a affects myocardial cell apoptosis by regulating the activation and inactivation of the Wnt/β-catenin signaling pathway.
Insights
Micro ribonucleic acid-34a (miR-34a) promotes myocardial cell apoptosis after myocardial infarction (MI) by regulating the Wnt/β-catenin pathway. Inhibiting miR-34a reduces apoptosis and cardiac injury in a rat MI model.
Area of Science:
- Molecular Biology
- Cardiovascular Research
- Cellular Signaling
Background:
- Myocardial infarction (MI) leads to significant myocardial cell apoptosis.
- Micro ribonucleic acid-34a (miR-34a) is implicated in cellular stress responses.
- The Wnt/β-catenin signaling pathway plays a role in cardiac cell survival and death.
Purpose of the Study:
- To elucidate the molecular mechanism of miR-34a in promoting myocardial cell apoptosis in a rat model of MI.
- To investigate the role of the Wnt/β-catenin signaling pathway in miR-34a-mediated apoptosis.
Main Methods:
- Construction of a rat model of myocardial infarction (MI) using left anterior descending branch ligation.
- In vivo assessment using echocardiography, MRI, PCR, Western blotting, and H&E staining.
- In vitro studies using H9C2 cells under hypoxic conditions, with miR-34a inhibitors and Wnt/β-catenin pathway inhibitors.
Main Results:
- Inhibition of miR-34a significantly reduced myocardial cell apoptosis, decreased Caspase-3 levels, and improved cardiac function (EF, FS) in MI rats.
- miR-34a inhibition led to increased Wnt/β-catenin signaling pathway activation in MI rats.
- In vitro experiments confirmed that miR-34a promotes apoptosis, and this effect is mediated through the Wnt/β-catenin pathway.
Conclusions:
- miR-34a plays a crucial role in promoting myocardial cell apoptosis following myocardial infarction.
- The pro-apoptotic effect of miR-34a is achieved by regulating the Wnt/β-catenin signaling pathway.
- Targeting miR-34a represents a potential therapeutic strategy for mitigating cardiac injury after MI.
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