Key Laboratory of Atherosclerosis in Universities of Shandong, Taishan Medical University, Taian, China.
Lipids Health Dis. 2012 Sep 17;11:118. doi: 10.1186/1476-511X-11-118.
The single and combined effects of scavenger receptor-BI (SR-BI), ATP-binding cassette transporter (ABC) A1 and G1 on cholesterol efflux from Chinese Hamster Ovary (CHO) cells were investigated.
When apolipoproteinA-I (apoA-I) was used as an acceptor, ABCA1 overexpression led to an increase in total cholesterol (TC) in medium which is attributable to a 2-fold increase in free cholesterol (FC) content. When high-density lipoprotein 3 (HDL3) was used as an acceptor, SR-BI overexpression not only promoted FC efflux, but also promoted the uptake of cholesteryl ester (CE) 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.
We found SR-BI associates with ABCG1 and inhibits ABCG1-mediated cholesterol efflux from cells to HDL3.
本研究旨在探讨清道夫受体 BI（SR-BI）、三磷酸腺苷结合盒转运体（ABC）A1 和 G1 对中国仓鼠卵巢（CHO）细胞胆固醇外排的单一和联合作用。
当载脂蛋白 A-I（apoA-I）作为接受体时，ABCA1 的过表达导致培养基中总胆固醇（TC）的增加，这归因于游离胆固醇（FC）含量增加了 2 倍。当高密度脂蛋白 3（HDL3）作为接受体时，SR-BI 的过表达不仅促进了 FC 的外排，而且促进了胆固醇酯（CE）进入细胞，导致培养基中 TC 无变化。ABCG1 的过表达增加了培养基中 FC 和 CE 的水平。然而，当 apoA-I 和 HDL3 均作为接受体时，SR-BI 的共表达对 ABCA1 介导的培养基中 FC 和 TC 积累增加没有影响。有趣的是，SR-BI 与 ABCG1 的共表达阻断了 ABCG1 介导的胆固醇向 HDL3 的外排，主要是通过促进 CE 从培养基中的再摄取。此外，共免疫沉淀实验表明，在过表达 ABCG1 和 SR-BI 的 BHK 细胞中，SR-BI 与 ABCG1 相互作用。
我们发现 SR-BI 与 ABCG1 相关，并抑制 ABCG1 介导的细胞胆固醇向 HDL3 的外排。
