The atherogenic actions of LPC on vascular smooth muscle cells and its LPA receptor mediated mechanism

被引:26
作者
Bao, Liang [1 ,2 ]
Qi, Jingwei [3 ]
Wang, Yue-wu [1 ]
Xi, Qilemuge [1 ]
Tserennadmid, Tseveensuren [1 ]
Zhao, Peng-fei [1 ]
Qi, Jerry [4 ]
Damirin, Alatangaole [1 ]
机构
[1] Inner Mongolia Univ, Sch Life Sci, Hohhot 010070, Peoples R China
[2] Hohhot Vocat Coll, Coll Biochem Engn, Hohhot 010051, Peoples R China
[3] Univ Calif Los Angeles, David Geffen Sch Med, Div Hematol Oncol, Dept Med, Los Angeles, CA 90095 USA
[4] Univ Calif Los Angeles, Coll Letters & Sci, Los Angeles, CA 90095 USA
基金
中国国家自然科学基金;
关键词
Lysophosphatidylcholine; Atherogenic actions; Lysophosphatidic acid receptor 1; Autotaxin; Human artery smooth muscle cells; LOW-DENSITY-LIPOPROTEIN; RETRACTED ARTICLE. SEE; LYSOPHOSPHOLIPASE-D; LYSOPHOSPHATIDIC ACIDS; AUTOTAXIN; G2A; CHEMOTAXIS; ACTIVATION; EXPRESSION; SERUM;
D O I
10.1016/j.bbrc.2018.07.135
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Lysophosphatidylcholine (LPC) is a bioactive lipid constituent of oxidized low density lipoprotein (ox-LDL). It regulates various cellular functions, including migration of circulating monocytes, expression of endothelial adhesion molecules, proliferation and migration of vascular smooth muscle cells (VSMCs). LPC can also be hydrolyzed into lysophosphatidic acid (LPA) by autotaxin (ATX) which possesses lysophospholipase D (lyso-PLD) activity. The aim of this study was to explore the effects of LPC on proliferation and migration of human artery smooth muscle cells (HASMCs) and the involvement of LPC-ATX-LPA pathway in these processes. In vitro, we found that LPC and LPA stimulated HASMCs proliferation and migration. Knockdown of LPA1 by siRNA and inhibit Gi protein with pertussis toxin (PTX) showed the contrary results. Silencing of LPC receptor genes did not significantly affect the LPC induced proliferation and migration. We detected the higher expressed mRNA and protein of ATX in HASMCs, and measured lyso-PLD activity. In atherosclerotic rabbit model, we observed high LPC level and high lyso-D activity in blood, and high expression of LPA1 in aorta walls. We also found that neointima appeared to be thickened and mRNA expressions of LPA1 appeared to be increased. These results revealed that LPC was converted into LPA by ATX to induce the proliferation and migration in HASMCs through LPA1/Gi/o/MAP Kinase signaling pathway. Our research suggested that LPC-ATX-LPA system contributed to the atherogenic action induced by ox-LDL. LPA1 antagonist may be considered as a potential therapeutic and preventative drug for cardiovascular disease. (C) 2018 Elsevier Inc. All rights reserved.
引用
收藏
页码:1911 / 1918
页数:8
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