Investigating the expression of miRNA-133 in animal models of myocardial infarction and its effect on cardiac function

X.-G. Zhang, L.-Q. Wang, H.-L. Guan

Nursing Department, Weifang People’s Hospital, Weifang, P.R. China. ht7qay@163.com

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• Cardiology

OBJECTIVE: This study aimed to investigate the expression of miR-133 in animal models of myocardial infarction and its effect on cardiac function.

MATERIALS AND METHODS: Forty-five male-specific pathogen-free (SPF) C57/BL6 mice were selected, among which 35 were made for animal models of myocardial infarction and were enrolled into Model Group and another 10 were enrolled into Blank Control Group. Seven mice died in the model making. Ten mice randomly selected from the 28 mice successfully modeled were transfected with adenovirus carrying miRNA-133 and set as Virus Group, while the remaining 18 mice were randomly divided into Virus No-load Group and Model Group. Mice in Virus Group were transfected with adenovirus carrying miRNA-133, while those in Virus No-load Group were transfected with empty viral vectors without miRNA-133. The left ventricular ejection fraction (LVEF) and fractional shortening (FS) of the mice weeks after the infection were recorded and evaluated by echocardiography. The relative expression levels of miR-133 in the heart tissues of the four groups of mice were compared by Real Time-Polymerase Chain Reaction (RT-PCR).

RESULTS: The miR-133 expressions in Blank Control Group and Virus Group were higher than that of Model Group (p<0.05). Then, the myocardial infarction area of mice was compared. The LVEF and FS values of mice in Model Group, Virus No-load Group, and Virus Group were significantly lower than those in Blank Control Group, with the LVEF and FS values of Virus Group higher than that of Model Group and Virus No-load Group (p<0.05). The swimming time of Blank Control Group was significantly higher than that of Model Group and Virus Group (p<0.05), with Virus Group and Virus No-load Group having a greatly longer swimming time than Model Group (p<0.05). The myocardial infarction area of mice in Virus Group was significantly smaller than that in Model Group and Virus No-load Group, the difference was statistically significant (p<0.05). There was no significant difference in myocardial infarction area of mice between Model Group and Virus No-load Group (p>0.05).

CONCLUSIONS: MiR-133 was in a low expression state in the mice models of myocardial infarction and the overexpression of miR-133 could significantly improve the cardiac function index and motor function, as well as reduce the myocardial infarction area of mice with myocardial infarction. This could inspire new molecular therapy for the treatment of myocardial infarction.

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