Int J Sports Med 2020; 41(07): 475-483
DOI: 10.1055/a-1018-1902
Training & Testing

Inhibiting MicroRNA-497 Improves the Effects of Exercise Training on Myocardial Infarction

Zhenci Li
1   Department of Cardiology, Guangzhou First People’s Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China
,
Jing Lv
2   Department of Anesthesiology, Guangzhou First People’s Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China
,
Yizhi Pan
1   Department of Cardiology, Guangzhou First People’s Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China
,
Yi Luo
1   Department of Cardiology, Guangzhou First People’s Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China
,
Zhen Liu
1   Department of Cardiology, Guangzhou First People’s Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China
,
Jiankai Huang
1   Department of Cardiology, Guangzhou First People’s Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China
,
Qi Wu
1   Department of Cardiology, Guangzhou First People’s Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China
› Author Affiliations
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Abstract

Exercise training (ET) could improve myocardial infarction (MI), and microRNA-497 is highly associated with MI. This study aimed to investigate whether the regulation of miR-497 is involved in the positive effects of ET on MI. MI rat models induced by left anterior descending (LAD) were subjected to interval training and infarct size was observed. Blood and myocardial samples were collected from the rats for determining the expressions of miR-497. To evaluate the functions of miR-497, miR-497 agomir and antagomir were injected accordingly into grouped rats during ET, and subsequently, the expressions of apoptotic and inflammatory factors were determined. ET reduced the infarct size in MI rats and inhibited the levels of miR-497. MiR-497 agomir injection enlarged the infarct size, and reversed the shrunk infarct size induced by ET. However, miR-497 antagomir further promoted the positive effect on MI improved by ET. Chloride voltage-gated channel 3 (CLCN3) was identified as the most possible target for miR-497. Moreover, ET improving MI also involved the regulation of apoptotic and inflammatory factors. The mechanisms underlying the positive effects of ET on MI were highly associated with the regulation of miR-497.



Publication History

Received: 00 00 2019

Accepted: 16 September 2019

Article published online:
11 March 2020

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