Open AccessC1q/ TNF ‐related protein 9 inhibits the cholesterol‐induced Vascular smooth muscle cell phenotype switch and cell dysfunction by activating AMP‐dependent kinase
Author(s) -
Liu Qi,
Zhang Hui,
Lin Jiale,
Zhang Ruoxi,
Chen Shuyuan,
Liu Wei,
Sun Meng,
Du Wenjuan,
Hou Jingbo,
Yu Bo
Publication year - 2017
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13196
Subject(s) - ampk , vascular smooth muscle , cholesterol , downregulation and upregulation , microbiology and biotechnology , endocrinology , medicine , chemistry , cholesterol 7 alpha hydroxylase , adipokine , protein kinase a , foam cell , lipid metabolism , cancer research , biology , kinase , biochemistry , lipoprotein , gene , leptin , smooth muscle , obesity
Vascular smooth muscle cells ( VSMC s) switch to macrophage‐like cells after cholesterol loading, and this change may play an important role in the progression of atherosclerosis. C1q/ TNF ‐related protein 9 ( CTRP 9) is a recently discovered adipokine that has been shown to have beneficial effects on glucose metabolism and vascular function, particularly in regard to cardiovascular disease. The question of whether CTRP 9 can protect VSMC s from cholesterol damage has not been addressed. In this study, the impact of CTRP 9 on cholesterol‐damaged VSMC s was observed. Our data show that in cholesterol‐treated VSMC s, CTRP 9 significantly reversed the cholesterol‐induced increases in pro‐inflammatory factor secretion, monocyte adhesion, cholesterol uptake and expression of the macrophage marker CD 68. Meanwhile, CTRP 9 prevented the cholesterol‐induced activation of the TLR 4–MyD88–p65 pathway and upregulated the expression of proteins important for cholesterol efflux. Mechanistically, as si RNA ‐induced selective gene ablation of AMPK α1 abolished these effects of CTRP 9, we concluded that CTRP 9 achieves these protective effects in VSMC s through the AMP‐dependent kinase (AMPK) pathway.