Suining Xu, Lihua Li, Jinchuan Yan, Fei Ye, Chen Shao, Zhen Sun, Zhengyang Bao, Zhiyin Dai, Jie Zhu, Lele Jing, Zhongqun Wang
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 2017 Nov 08Among the various complications of type 2 diabetes mellitus, atherosclerosis causes the highest disability and morbidity. A multitude of macrophage-derived foam cells are retained in atherosclerotic plaques resulting not only from recruitment of monocytes into lesions but also from a reduced rate of macrophage migration from lesions. Nε-carboxymethyl-Lysine (CML), an advanced glycation end product, is responsible for most complications of diabetes. This study was designed to investigate the mechanism of CML/CD36 accelerating atherosclerotic progression via inhibiting foam cell migration. In vivo study and in vitro study were performed. For the in vivo investigation, CML/CD36 accelerated atherosclerotic progression via promoting the accumulation of macrophage-derived foam cells in aorta and inhibited macrophage-derived foam cells in aorta migrating to the para-aorta lymph node of diabetic apoE-/- mice. For the in vitro investigation, CML/CD36 inhibited RAW264.7-derived foam cell migration through NOX-derived ROS, FAK phosphorylation, Arp2/3 complex activation and F-actin polymerization. Thus, we concluded that CML/CD36 inhibited foam cells of plaque migrating to para-aorta lymph nodes, accelerating atherosclerotic progression. The corresponding mechanism may be via free cholesterol, ROS generation, p-FAK, Arp2/3, F-actin polymerization. Copyright © 2017 Elsevier Masson SAS. All rights reserved.
Suining Xu, Lihua Li, Jinchuan Yan, Fei Ye, Chen Shao, Zhen Sun, Zhengyang Bao, Zhiyin Dai, Jie Zhu, Lele Jing, Zhongqun Wang. CML/CD36 accelerates atherosclerotic progression via inhibiting foam cell migration. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2017 Nov 08;97:1020-1031
PMID: 29136780
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