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RASSF1 promotes cardiomyocyte apoptosis after acute myocardial infarction and is regulated by miR‐125b
Author(s) -
Xiaochuan Bai,
Qianfeng Jiang,
Min Xu,
Xiao Liang
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29236
Subject(s) - apoptosis , myocardial infarction , downregulation and upregulation , in vivo , hypoxia (environmental) , in vitro , medicine , cancer research , microbiology and biotechnology , chemistry , biology , biochemistry , organic chemistry , oxygen , gene
Cardiomyocyte apoptosis is a common pathological injury in association with acute myocardial infarction (AMI). In the current study, the relationship between Ras‐association domain family 1 (RASSF1) and cardiomyocyte apoptosis was investigated. RASSF1 was significantly over expressed in infarcted myocardial tissues as well as in cardiomyocytes induced by hypoxia. Inhibition of RASSF1 expression alleviated cardiomyocytes apoptosis induced by hypoxia in vitro and reduced cardiomyocytes apoptosis after AMI in vivo. RASSF1 expression was directly modulated by miR‐125b, which was further confirmed by luciferase reporter assay. The current study verified that the miR‐125b/RASSF1 axis was involved in cardiomyocytes apoptosis. To sum up, these results suggest that RASSF1 downregulation alleviated infarction‐induced cardiomyocytes apoptosis and was regulated by miR‐125b.