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作者

Song, GH Zong, CL Liu, Q Si, YH Liu, J Li, W Zhu, P Qin, SC

作者单位

Peoples Liberat Army Gen Hosp, Beijing, Peoples R China        Chinese People's Liberation Army General Hospital Taishan Med Univ, Inst Atherosclerosis, Key Lab Atherosclerosis Univ Shandong, Tai An, Shandong, Peoples R China        Taishan Medical University

刊名

LIPIDS IN HEALTH AND DISEASE

年份

2012

卷号

Vol.11

ISSN

1476-511X

关键词

RECEPTOR CLASS-B ATHEROSCLEROTIC LESION DEVELOPMENT MARROW-DERIVED CELLS CELLULAR CHOLESTEROL PLASMA HDL APOA-I ABCA1 TRANSPORT BINDING MICE

摘要

Background: The single and combined effects of scavenger receptor-BI , ATP-binding cassette transporter A1 and G1 on cholesterol efflux from Chinese Hamster Ovary cells were investigated. Results: When apolipoproteinA-I was used as an acceptor, ABCA1 overexpression led to an increase in total cholesterol in medium which is attributable to a 2-fold increase in free cholesterol content. When high-density lipoprotein 3 was used as an acceptor, SR-BI overexpression not only promoted FC efflux,...更多

Background: The single and combined effects of scavenger receptor-BI , ATP-binding cassette transporter A1 and G1 on cholesterol efflux from Chinese Hamster Ovary cells were investigated. Results: When apolipoproteinA-I was used as an acceptor, ABCA1 overexpression led to an increase in total cholesterol in medium which is attributable to a 2-fold increase in free cholesterol content. When high-density lipoprotein 3 was used as an acceptor, SR-BI overexpression not only promoted FC efflux, but also promoted the uptake of cholesteryl ester into cells, resulting in no TC varieties in medium. Overexpression of ABCG1 increased both the FC and CE levels in medium. However, when apoA-I and HDL3 were both used as acceptors, coexpression of SR-BI has no effect on ABCA1-mediated increased FC and TC accumulation in medium. Interestingly, coexpression of SR-BI with ABCG1 blocked the ABCG1-mediated cholesterol efflux to HDL3, mostly by promoting the reuptake of CE from the medium. Furthermore, co-immunoprecipitation experiments revealed that SR-BI interacted with ABCG1 in BHK cells overexpressing ABCG1 and SR-BI. Conclusions: We found SR-BI associates with ABCG1 and inhibits ABCG1-mediated cholesterol efflux from cells to HDL3.收起

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