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microRNA‐132 inhibits cardiomyocyte apoptosis and myocardial remodeling in myocardial infarction by targeting IL‐1β
Author(s) -
Zhao Zonglei,
Du Song,
Shen Shuxin,
Wang Lixia
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29175
Subject(s) - ventricle , downregulation and upregulation , ventricular remodeling , myocardial infarction , apoptosis , ejection fraction , medicine , microrna , cardiology , cardiac function curve , heart failure , chemistry , biochemistry , gene
Abstract The patients suffering from myocardial infarction (MI) undergo cardiac remodeling with the features of expanded myocardial infarct size and dilated left ventricle. Multiple microRNAs (miRNAs) are emerged as crucial modulators to participate in the remodeling process. This study is mainly intended to clarify the regulatory mechanism of miR‐132 in the MI‐induced myocardial remodeling. miR‐132 low expression, while interleukin‐1β (IL‐1β) high expression was determined in MI by reverse‐transcription quantitative polymerase chain reaction and ELISA assays. MI rats showed decreased cardiac function and increased cardiomyocyte apoptosis. Moreover, miR‐132 and IL‐1β levels were altered in cardiomyocytes to explore their role in MI, with levels of proapoptotic or antiapoptotic proteins in MI together with cardiac function indexes observed. In addition, upregulation of miR‐132, decreased levels of Bax and Cleaved Caspase‐3, increased left ventricular ejection fraction, left ventricular fractional shortening, the maximum rate of rise or decrease of left ventricular pressure (±dp/dt max ), and Bcl‐2 level, which could be reversed by overexpressing IL‐1β. All in all, miR‐132 inhibits cardiomyocyte apoptosis so as to ameliorate myocardial remodeling in rats with MI through IL‐1β downregulation. Thus, miR‐132 is a potential candidate for the MI treatment.