作者: Jane V. MULCAHY , Dave R. RIDDELL , James S. OWEN
DOI: 10.1042/BJ20030307
关键词:
摘要: Although studies in recombinant cells indicate that scavenger receptor class B, type I (SR-BI) can promote cholesterol efflux, investigations transgenic mice overexpressing or deficient SR-BI endorse its physiological function as selectively sequestering cholesteryl esters from high-density lipoproteins (HDLs). Less clear is the role of SR-BII, a splice variant SR-B gene differs only C-terminal cytoplasmic domain. Here, we identify several putative signalling motifs C-terminus human which are absent SR-BI, and hypothesize these interact with molecules to mobilize stored and/or efflux intracellular free cholesterol. 'Pull-down' assays using panel tagged SH3 (Src homology 3) domains showed but not bound domain phospholipase C-gamma1; this interaction was not, however, detected under more conditions. Specific anti-peptide antisera identified SR-BII monocyte/macrophage THP-1 and, cells, revealed localization caveolae, plasma membrane microdomain concentrates signal-transducer acts conduit for flux between lipoproteins. Consistent caveolar localization, expression Chinese hamster ovary (CHO-SR-BII) associated increased HDL-mediated efflux. Nevertheless, when CHO-SR-BII were pre-loaded [(3)H]oleate incubated HDL, ester stores reduced compared control cells. We conclude although expressed by macrophages, contains localizes ability stimulate does reflect enhanced hydrolysis esters.