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Published on: June 3, 2018
MicroRNA-150 alleviates acute myocardial infarction through regulating cardiac fibroblasts in ventricular remodeling
1Department of Cardiology, Jinan Central Hospital Affiliated to Shandong University, Jinan, China. gttstg@163.com.
Objective:
The aim of this study was to investigate the effect of microRNA-150 on the regulation of myocardial fibrosis and ventricular remodeling in rats with acute myocardial infarction (AMI).
Materials And Methods:
The AMI rats model was established by the ligation of the left anterior descending coronary artery (LAD) in vivo. After AMI procedures, the rats were injected with microRNA-150 lentivirus overexpression or negative control, respectively. Cardiac function of rats was evaluated by echocardiography. Hematoxylin and eosin (HE) staining and Masson trichrome were performed to evaluate myocardial fibrosis in each rat. Meanwhile, cardiomyocyte apoptosis was detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) method. The expression levels of microRNA-150, col1α1, col1α2, col3 and α smooth muscle actin (α-SMA) in the border zone of rat infarct myocardium were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot, respectively.
Results:
MicroRNA-150 expression in the border zone of infarct myocardium decreased significantly at day 28 after AMI (p<0.05). Overexpressing microRNA-150 significantly improved cardiac function, decreased collagen volume fraction (CVF) and attenuated cardiomyocyte apoptosis in rats. Furthermore, the expression levels of col1ɑ1, col1ɑ2, col3 and α-SMA in the border zone of infarct myocardium were remarkably down-regulated in rats overexpressing microRNA-150 compared with those of controls (p<0.001).
Conclusions:
MicroRNA-150 expression in the border zone of rat infarct myocardium decreased at day 28 after AMI. In addition, the upregulation of microRNA-150 in myocardial tissue could inhibit myocardial fibrosis and improve ventricular remodeling at post-AMI.
Insights
Upregulating microRNA-150 in rats after acute myocardial infarction (AMI) reduced myocardial fibrosis and improved cardiac function. This microRNA plays a key role in regulating ventricular remodeling post-AMI.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Biomedical Science
Background:
- Acute myocardial infarction (AMI) leads to significant myocardial fibrosis and adverse ventricular remodeling.
- MicroRNAs are critical regulators of cardiac pathophysiology, but their specific roles in post-AMI remodeling require further elucidation.
Purpose of the Study:
- To investigate the role of microRNA-150 in regulating myocardial fibrosis and ventricular remodeling in a rat model of AMI.
- To determine the therapeutic potential of microRNA-150 upregulation in mitigating post-infarction cardiac dysfunction.
Main Methods:
- An acute myocardial infarction (AMI) rat model was established using left anterior descending coronary artery ligation.
- Rats received lentiviral vectors for microRNA-150 overexpression or a negative control.
- Cardiac function was assessed via echocardiography; myocardial fibrosis was quantified using HE and Masson trichrome staining.
- Cardiomyocyte apoptosis was detected by TUNEL assay, and gene/protein expression (col1α1, col1α2, col3, α-SMA) was analyzed by qRT-PCR and Western blot.
Main Results:
- MicroRNA-150 expression was significantly decreased in the infarct border zone 28 days post-AMI.
- Overexpression of microRNA-150 significantly improved cardiac function and reduced collagen volume fraction (CVF).
- MicroRNA-150 upregulation attenuated cardiomyocyte apoptosis and markedly downregulated fibrosis-related markers (col1α1, col1α2, col3, α-SMA).
Conclusions:
- MicroRNA-150 levels are reduced in rat myocardium following AMI.
- Upregulating microRNA-150 in myocardial tissue effectively inhibits myocardial fibrosis and promotes favorable ventricular remodeling post-AMI.
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