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miR‐497 accelerates oxidized low‐density lipoprotein‐induced lipid accumulation in macrophages by repressing the expression of apelin
Author(s) -
Cui Junfeng,
Ren Zhong,
Zou Wenshuang,
Jiang Yanling
Publication year - 2017
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.10808
Subject(s) - apelin , downregulation and upregulation , foam cell , chemistry , macrophage , microrna , lipoprotein , thp1 cell line , microbiology and biotechnology , cholesterol , lipid metabolism , pathogenesis , endocrinology , medicine , cell culture , biology , biochemistry , receptor , gene , in vitro , genetics
microRNAs (miRNAs) play important roles in the pathogenesis of atherosclerosis. A previous study has reported that miR‐497 is elevated in advanced atherosclerotic lesions in an apoE‐deficient ( apoE ‐/‐) mouse model. The purpose of this study is to test whether miR‐497 can modulate macrophage foam cell formation, an initiating event in atherosclerosis. We found that miR‐497 was upregulated in THP‐1 macrophages after treatment with oxidized low‐density lipoprotein (oxLDL). Enforced expression of miR‐497 promoted lipid accumulation and decreased cholesterol efflux in oxLDL‐exposed THP‐1 macrophages. In contrast, downregulation of miR‐497 suppressed oxLDL‐induced lipid accumulation in THP‐1 macrophages. Apelin was identified to be a downstream target of miR‐497. Overexpression of miR‐497 significantly reduced the expression of apelin in THP‐1 macrophages. Interestingly, delivery of a miR‐497‐resistant variant of apelin significantly inhibited lipid accumulation and enhanced cholesterol efflux in miR‐497‐overexpressing THP‐1 macrophages in response to oxLDL. In addition, miR‐497 expression was increased and negatively correlated with apelin protein expression in human atherosclerotic lesions. In conclusion, miR‐497 contributes to oxLDL‐induced lipid deposition in macrophages largely via targeting of apelin and thus represents a potential therapeutic target for atherosclerosis.