Angiopoietin-1 aggravates atherosclerosis by inhibiting cholesterol efflux and promoting inflammatory response

ABCG1公司 ABCA1 胆固醇逆向转运 炎症 载脂蛋白E 胆固醇 化学 体内 下调和上调 巨噬细胞 内科学 内分泌学 医学 流出 生物 脂蛋白 免疫学 体外 生物化学 运输机 生物技术 基因 疾病
作者
Xiang Ou,Jiahui Gao,Lin-Hao He,Xiao-Hua Yu,Gang Wang,Jin Zou,Zhen-Wang Zhao,Dawei Zhang,Zhi-jiao Zhou,Chao‐Ke Tang
出处
期刊:Biochimica Et Biophysica Acta - Molecular And Cell Biology Of Lipids [Elsevier]
卷期号:1865 (2): 158535-158535 被引量:29
标识
DOI:10.1016/j.bbalip.2019.158535
摘要

Abstract Objective Angiopoietin-1 (Ang-1), a secreted protein, mainly regulates angiogenesis. Ang-1 has been shown to promote the development of atherosclerosis, whereas little is known about its effects on lipid metabolism and inflammation in this process. Method Ang-1 was transfected into ApoE−/− mice via lentiviral vector or incubated with THP-1 derived macrophages. Oil red O and HE staining were performed to measure the size of atherosclerotic plaques in ApoE−/− mice. Immunofluorescence was employed to show the expression of target proteins in aorta. [3H] labeled cholesterol was performed to examine the efficiency of cholesterol efflux and reverse cholesterol transport (RCT) both in vivo and vitro. Western blot and qPCR were used to quantify target proteins both in vivo and vitro. ELISA detected the levels of pro-inflammatory cytokines in mouse peritoneal macrophage. Results Our data showed that Ang-1 augmented atherosclerotic plaques formation and inhibited cholesterol efflux. The binding of Ang-1 to Tie2 resulted in downregulation of LXRα, ABCA1 and ABCG1 expression via inhibiting the translocation of TFE3 into nucleus. In addition, Ang-1 decreased serum HDL-C levels and reduced reverse cholesterol transport (RCT) in ApoE−/− mice. Furthermore, Ang-1 induced lipid accumulation followed by increasing TNF-α, IL-6, IL-1β,and MCP-1 produced by MPMs, as well as inducing M1 phenotype macrophage marker iNOS and CD86 expression in aorta of ApoE−/− mice. Conclusion Ang-1 has an adverse effect on cholesterol efflux by decreasing the expression of ABCA1 and ABCG1 via Tie2/TFE3/LXRα pathway, thereby promoting inflammation and accelerating atherosclerosis progression.
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