An oxidized lipid-peroxisome proliferator-activated receptor γ-chemokine pathway in the regulation of macrophage-vascular smooth muscle cell adhesion

被引：24
作者：
Barlic, Jana
Murphy, Philip M.
机构：
[1] Imperial Coll London, Fac Med, Natl Heart & Lung Inst, Leukocyte Biol Sect, London SW7 2AZ, England
[2] NIH, NIAID, Immunol Mol Lab, Mol Signaling Sect, Bethesda, MD 20892 USA
来源：
TRENDS IN CARDIOVASCULAR MEDICINE | 2007年 / 17卷 / 08期
关键词：
D O I：
10.1016/j.tcm.2007.09.004
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Recent genetic studies have implicated pro-inflammatory chemokines and chemokine receptors in atherogenesis. Studies at the molecular and cellular levels have suggested specific atherogenic mechanisms for two chemokine-chemokine receptor pairs, CCL2-CCR2 and CX3CL1-CX3CR1, involving differential receptor regulation by the transcription factor peroxisome proliferator-activated receptor gamma. This pathway is triggered by oxidized proatherogenic lipids, such as oxidized low-density lipoprotein and linoleic acid derivatives, which promote differentiation of CCR2(hi)CX3CRI(lo) human monocytes to CCR2(lo)CX3CR1(hi) macrophages that adhere to coronary artery smooth muscle cells in a CX3CR1- and peroxisome proliferator-activated receptor gamma-dependent manner. Switching CX3CR1 on and CCR2 off in vivo may result in cessation of CCR2-dependent migration and activation of CX3CR1-dependent retention that together may promote foam cell accumulation in the vessel wall.
引用
收藏
页码：269 / 274
页数：6
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