de la Llera-Moya M, Rothblat G H, Connelly M A, Kellner-Weibel G, Sakr S W, Phillips M C, Williams D L
Department of Biochemistry, MCP diamond Hahnemann School of Medicine, Philadelphia PA, 19129, USA.
J Lipid Res. 1999 Mar;40(3):575-80.
In addition to its effect on high density lipoprotein (HDL) cholesteryl ester (CE) uptake, scavenger receptor BI (SR-BI) was recently reported to stimulate free cholesterol (FC) flux from Chinese hamster ovary (CHO) cells stably expressing mouse SR-BI, a novel function of SR-BI that may play a role in cholesterol removal from the vessel wall where the receptor can be found. It is possible that SR-BI stimulates flux simply by tethering acceptor HDL particles in close apposition to the cell surface thereby facilitating the movement of cholesterol between the plasma membrane and HDL. To test this, we used transiently transfected cells and compared the closely related class B scavenger receptors mouse SR-BI and rat CD36 for their ability to stimulate cholesterol efflux as both receptors bind HDL with high affinity. The results showed that, although acceptor binding to SR-BI may contribute to efflux to a modest extent, the major stimulation of FC efflux occurs independently of acceptor binding to cell surface receptors. Instead our data indicate that SR-BI mediates alterations to membrane FC domains which provoke enhanced bidirectional FC flux between cells and extracellular acceptors.
除了对高密度脂蛋白（HDL）胆固醇酯（CE）摄取有影响外，最近有报道称清道夫受体BI（SR-BI）可刺激稳定表达小鼠SR-BI的中国仓鼠卵巢（CHO）细胞的游离胆固醇（FC）流出，这是SR-BI的一种新功能，可能在从可发现该受体的血管壁清除胆固醇中发挥作用。SR-BI可能只是通过将受体HDL颗粒紧密连接在细胞表面，从而促进胆固醇在质膜和HDL之间的移动来刺激流出。为了验证这一点，我们使用了瞬时转染细胞，并比较了密切相关的B类清道夫受体小鼠SR-BI和大鼠CD36刺激胆固醇流出的能力，因为这两种受体都以高亲和力结合HDL。结果表明，虽然受体与SR-BI的结合可能在一定程度上有助于流出，但FC流出的主要刺激发生与受体与细胞表面受体的结合无关。相反，我们的数据表明，SR-BI介导了膜FC结构域的改变，从而促进了细胞与细胞外受体之间双向FC流出的增强。
