CML/CD36 accelerates atherosclerotic progression via inhibiting foam cell migration.

Autor: Xu S; Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China. Electronic address: amyxsn@outlook.com., Li L; Department of Pathology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China. Electronic address: wzhnanhua@126.com., Yan J; Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China. Electronic address: yanjinchuan@hotmail.com., Ye F; Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China. Electronic address: peteryefei@163.com., Shao C; Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China. Electronic address: shaochen84@163.com., Sun Z; Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China. Electronic address: 1398041019@qq.com., Bao Z; Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China. Electronic address: 490213060@qq.com., Dai Z; Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China. Electronic address: 328991181@qq.com., Zhu J; Department of Cardiology, Luan Affiliated Hospital of Anhui Medical University, Anhui 237005, China. Electronic address: zhujiemed@hotmail.com., Jing L; Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China. Electronic address: 459736150@qq.com., Wang Z; Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China. Electronic address: wangtsmc@aliyun.com.
Jazyk: angličtina
Zdroj: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie [Biomed Pharmacother] 2018 Jan; Vol. 97, pp. 1020-1031. Date of Electronic Publication: 2017 Nov 08.
DOI: 10.1016/j.biopha.2017.11.041
Abstrakt: Among 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.)
Databáze: MEDLINE
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