| First Author | Ji A | Year | 2011 |
| Journal | Atherosclerosis | Volume | 217 |
| Issue | 1 | Pages | 106-12 |
| PubMed ID | 21481393 | Mgi Jnum | J:220507 |
| Mgi Id | MGI:5634884 | Doi | 10.1016/j.atherosclerosis.2011.03.017 |
| Citation | Ji A, et al. (2011) Scavenger receptor SR-BI in macrophage lipid metabolism. Atherosclerosis 217(1):106-12 |
| abstractText | OBJECTIVE: To investigate the mechanisms by which macrophage scavenger receptor BI (SR-BI) regulates macrophage cholesterol homeostasis and protects against atherosclerosis. METHODS AND RESULTS: The expression and function of SR-BI was investigated in cultured mouse bone marrow-derived macrophages (BMM). SR-BI, the other scavenger receptors SRA and CD36 and the ATP-binding cassette transporters ABCA1 and ABCG1 were each distinctly regulated during BMM differentiation. SR-BI levels increased transiently to significant levels during culture. SR-BI expression in BMM was reversibly down-regulated by lipid loading with modified LDL; SR-BI was shown to be present both on the cell surface as well as intracellularly. BMM exhibited selective HDL CE uptake, however, this was not dependent on SR-BI or another potential candidate glycosylphosphatidylinositol anchored high density lipoprotein binding protein 1 (GPIHBP1). SR-BI played a significant role in facilitating bidirectional cholesterol flux in non lipid-loaded cells. SR-BI expression enhanced both cell cholesterol efflux and cholesterol influx from HDL, but did not lead to altered cellular cholesterol mass. SR-BI-dependent efflux occurred to larger HDL particles but not to smaller HDL(3). Following cholesterol loading, ABCA1 and ABCG1 were up-regulated and served as the major contributors to cholesterol efflux, while SR-BI expression was down-regulated. CONCLUSION: Our results suggest that SR-BI plays a significant role in macrophage cholesterol flux that may partly account for its effects on atherogenesis. |
