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Updated: Mar 20, 2026
Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery
Published on: August 16, 2019
[Relationship between myocardial microRNA-30a expression and myocardial fibrosis in rats post myocardial infarction]
1Department of Cardiology, Nanjing Hospital Affiliated to Nanjing Medical University, Nanjing 210006, China.
Objective:
To explore the potential role and mechanism of microRNA(miR)-30a in myocardial fibrosis after myocardial infarction (MI).
Methods:
Rats were randomly divided into 1 week MI group (n=11), 2 weeks MI group (n=13) and 4 weeks MI group (n=15) by applying random number table after left anterior descending coronary artery ligation. Rats in Sham group were examined at respective time points (n=16). Heart function was monitored by echocardiography. Myocardial collagen volume fraction (CVF) was determined on Masson stained sections. Myocardial expression of collagen Ⅰ and Ⅲ was determined by immunohistochemistry. The myocardial mRNA level of miR-30a, TGF-β1 and CTGF were detected by real time-quantitative PCR analysis. The myocardial protein levels of TGF-β1 and CTGF were measured by Western blot analysis.
Results:
The LVEDD ((8.37±0.58) mm) and LVESD ((6.12±0.82) mm) in 4 weeks MI group were significantly higher than those in Sham group ((6.08±0.57) mm, (4.17±0.60) mm), all P<0.01. The FS ((27.0±3.9) %) and LVEF ((51.0±6.3) %) in 4 weeks MI group were significantly lower than those in Sham group ((47.0±2.1) %, (82.0±2.3)%), all P<0.01. The level of myocardial CVF in 1 week MI group, 2 weeks MI group and 4 weeks MI group were significantly higher than in Sham group (all P<0.01) in a time-dependent manner. The level of myocardial collagen Ⅰ and Ⅲ was increased gradually from 1 week to 4 weeks post MI compared with Sham group (all P<0.01). The collagen Ⅰ/Ⅲ ratio was similar between 1 week MI group and Sham group (P=0.58), however, which was significantly higher in 2 weeks MI group and 4 weeks MI group compared with Sham group (all P<0.01), and the ratio was significantly higher in 4 weeks MI group than 2 weeks MI group (P<0.01). The level of miR-30a was significantly and gradually reduced in all MI groups compared with Sham group (all P<0.01). The mRNA and protein levels of TGF-β1 and CTGF were significantly and gradually increased after MI compared with Sham group (all P<0.001).
Conclusions:
Our results indicate that overexpression of miR-30a after MI might be a potential strategy for suppressing myocardial fibrosis by modulating the mRNA and protein levels of TGF-β1 and CTGF.
Insights
MicroRNA-30a (miR-30a) levels decrease after myocardial infarction (MI), promoting fibrosis. Overexpressing miR-30a may suppress this fibrosis by targeting TGF-β1 and CTGF, offering a potential therapeutic strategy.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Biomedical Science
Background:
- Myocardial infarction (MI) often leads to myocardial fibrosis, a significant cause of heart dysfunction.
- MicroRNAs (miRNAs) play crucial roles in post-MI cardiac remodeling and fibrosis.
- Understanding the specific roles of miRNAs like miR-30a is vital for developing targeted therapies.
Purpose of the Study:
- To investigate the role and mechanism of microRNA-30a (miR-30a) in the development of myocardial fibrosis following myocardial infarction (MI).
- To explore whether modulating miR-30a levels can impact fibrotic processes in the infarcted heart.
Main Methods:
- Rats underwent left anterior descending coronary artery ligation to induce MI, with groups assessed at 1, 2, and 4 weeks post-MI.
- Echocardiography monitored heart function, while Masson staining assessed collagen volume fraction (CVF).
- Immunohistochemistry, RT-qPCR, and Western blot analyzed collagen expression, and miR-30a, TGF-β1, and CTGF levels.
Main Results:
- MI induced significant cardiac dysfunction, increased myocardial CVF, and elevated collagen I and III expression in a time-dependent manner.
- miR-30a levels were significantly reduced post-MI, while mRNA and protein levels of TGF-β1 and CTGF were significantly increased.
- The collagen I/III ratio increased significantly at 2 and 4 weeks post-MI.
Conclusions:
- Reduced miR-30a expression is associated with the progression of myocardial fibrosis after MI.
- Modulating miR-30a levels, potentially through overexpression, could be a therapeutic strategy to suppress myocardial fibrosis.
- Targeting the TGF-β1 and CTGF pathways offers a mechanism for miR-30a's antifibrotic effects.
