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Medical Science Monitor Basic Research


eISSN: 1643-3750

The Role of MicroRNA-181a in Myocardial Fibrosis Following Myocardial Infarction in a Rat Model

Peng Chen, Jialin Pan, Xinming Zhang, Zhewei Shi, Xiangjun Yang

Department of Cardiology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China (mainland)

Med Sci Monit 2018; 24: LBR4121-4127

DOI: 10.12659/MSM.908056

Available online: 2018-06-16

Published: 2018-06-16


BACKGROUND: The role of miR-181a in the development of cardiac disease and in particular, myocardial fibrosis following myocardial infarction (MI) remains unknown. The aim of this study was to explore the role of miR-181a in myocardial fibrosis in a rat model of MI and the expression of TGF-β receptor III (TβRIII).
MATERIAL AND METHODS: Forty adult male Wistar rats were randomly divided into an MI model group (n=30) and a control group with (n=10). The rat MI model involved ligating the left anterior descending (LAD) coronary artery in the model group; the control group was treated with a sham operation. Cardiac function was assessed using cardiac ultrasound. Myocardial fibroblasts were extracted from the rat hearts and transfected with a miR-mimic or miR-inhibitor, and cell growth was measured using an MTT assay. The level of miR-181a expression was detected using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blots.
RESULTS: miR-181a expression was significantly increased during the progression of MI (P<0.05). Over-expression of miR-181a was associated with increased deposition of extracellular matrix (ECM) components, collagen I and fibronectin. This effect was reversed with the use of a miR-181a inhibitor (P<0.05). Upregulation of miR-181a suppressed the expression of TGF-β receptor III (TβRIII) by binding with 3’-UTR.
CONCLUSIONS: In this rat model of MI, the findings were that miR-181a had a role in the progression of myocardial fibrosis. The findings require further studies to determine whether miR-181a might provide a novel therapeutic target to limit myocardial fibrosis following MI.

Keywords: Endomyocardial Fibrosis, Myocardial Infarction