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miR‐16 exhibits protective function in LPS‐treated cardiomyocytes by targeting DOCK2 to repress cell apoptosis and exert anti‐inflammatory effect
Author(s) -
Wang Lei,
Zhang Yangyang,
Zhu Guangfu,
Ma Yuncong,
Zuo Huan,
Tian Xia
Publication year - 2020
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11371
Subject(s) - apoptosis , flow cytometry , lipopolysaccharide , myocarditis , microrna , western blot , downregulation and upregulation , viability assay , microbiology and biotechnology , cancer research , inflammation , cytokinesis , chemistry , cell , biology , immunology , medicine , gene , cell division , biochemistry
This study aims to investigate the effects of microRNA (miR)‐16/dedicator of cytokinesis 2 (DOCK2) on myocarditis. The differences in the expression of genes in acute myocarditis were filtered out across Gene Expression Omnibus (GEO) database. Myocarditis cell model was established by lipopolysaccharide (LPS) stimulation in cardiomyocytes. The association between miR‐16 and DOCK2 was predicted by bioinformatics software and confirmed by dual‐luciferase assay. Polymerase chain reaction and western blot analysis were employed to assess the expression levels of miR‐16 and DOCK2 under different conditions. Cells viability, apoptosis, and inflammatory reaction were evaluated by Cell Counting Kit‐8, flow cytometry, and enzyme‐linked immunosorbent assays. miR‐16, as an upstream regulator of DOCK2, exhibited lower expression in LPS‐induced myocarditis model. More importantly, we revealed that a marked augmentation of miR‐16 promoted the growth of LPS‐stimulated cardiomyocytes, and attenuated cell apoptosis and inflammatory response. However, an increasing expression of DOCK2 inhibited the remission of LPS‐induced myocardial injury caused by miR‐16 mimic. Herein, our results highlighted that upregulation of miR‐16 resulted in the protective effects on LPS‐induced myocardial injury by reducing DOCK2 expression, affording a pair of novel target molecules for ameliorating the symptoms of myocarditis.