CTRP6 inhibits PDGF-BB-induced vascular smooth muscle cell proliferation and migration

被引:53
|
作者
Dong, Xunzhong [1 ,2 ]
Hu, Hejie [1 ]
Fang, Zhengdong [1 ]
Cui, Jian [2 ]
Liu, Fangxin [3 ]
机构
[1] Anhui Med Univ, Affiliated Prov Hosp, Dept Vasc Surg, 17 Lujiang Rd, Hefei 230001, Anhui, Peoples R China
[2] Anhui Med Univ, Peoples Hosp Bozhou, Clin Coll, Dept Vasc Surg, Bozhou 236800, Anhui, Peoples R China
[3] Anhui Med Univ, Peoples Hosp Bozhou, Clin Coll, Dept Ultrasound, Bozhou 236800, Anhui, Peoples R China
关键词
CTRP6; Atherosclerosis; Vascular smooth muscle cell (VSMC); Migration; SPONTANEOUSLY HYPERTENSIVE-RATS; SIGNALING PATHWAY; PI3K/AKT/MTOR PATHWAY; ATHEROSCLEROSIS; EXPRESSION; AUTOPHAGY; AGONIST;
D O I
10.1016/j.biopha.2018.04.112
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Vascular smooth muscle cell (VSMC) proliferation and migration play critical roles in the development and progression of atherosclerosis. C1q/tumor necrosis factor-related protein 6 (CTRP6), a member of CTRPs family, was involved in cardiovascular diseases, inflammatory reaction and adipogenesis. However, the role of CTRP6 in VSMCs remains largely unknown. The purpose of this study is to investigate the effects of CTRP6 on VSMC proliferation and migration and explore the possible mechanism. Our results indicated that CTRP6 expression was dramatically down-regulated in human atherosclerotic tissues and in cultured VSMCs stimulated by platelet-derived growth factor-BB (PDGF-BB). In addition, CTRP6 overexpression significantly inhibited the proliferation and migration of VSMCs exposed to PDGF-BB, as well as increased expression of alpha-SMA and SM22 alpha in PDGF-BB-stimulated VSMCs. Furthermore, CTRP6 overexpression efficiently prevented the activation of PI3K/Akt/mTOR in VSMCs in response to PDGF-BB. In conclusion, these findings showed that CTRP6 inhibits PDGF-BB-induced VSMC proliferation and migration, at least in part, through suppressing the PI3K/Akt/mTOR signaling pathway. Therefore, CTRP6 may be a potential target for the treatment of atherosclerosis.
引用
收藏
页码:844 / 850
页数:7
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