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http://purl.uniprot.org/citations/21481393http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21481393http://www.w3.org/2000/01/rdf-schema#comment"

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."xsd:string
http://purl.uniprot.org/citations/21481393http://purl.org/dc/terms/identifier"doi:10.1016/j.atherosclerosis.2011.03.017"xsd:string
http://purl.uniprot.org/citations/21481393http://purl.uniprot.org/core/author"Cai L."xsd:string
http://purl.uniprot.org/citations/21481393http://purl.uniprot.org/core/author"Webb N.R."xsd:string
http://purl.uniprot.org/citations/21481393http://purl.uniprot.org/core/author"Meyer J.M."xsd:string
http://purl.uniprot.org/citations/21481393http://purl.uniprot.org/core/author"de Beer M.C."xsd:string
http://purl.uniprot.org/citations/21481393http://purl.uniprot.org/core/author"van der Westhuyzen D.R."xsd:string
http://purl.uniprot.org/citations/21481393http://purl.uniprot.org/core/author"Ji A."xsd:string
http://purl.uniprot.org/citations/21481393http://purl.uniprot.org/core/author"Akinmusire A."xsd:string
http://purl.uniprot.org/citations/21481393http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21481393http://purl.uniprot.org/core/name"Atherosclerosis"xsd:string
http://purl.uniprot.org/citations/21481393http://purl.uniprot.org/core/pages"106-112"xsd:string
http://purl.uniprot.org/citations/21481393http://purl.uniprot.org/core/title"Scavenger receptor SR-BI in macrophage lipid metabolism."xsd:string
http://purl.uniprot.org/citations/21481393http://purl.uniprot.org/core/volume"217"xsd:string
http://purl.uniprot.org/citations/21481393http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21481393
http://purl.uniprot.org/citations/21481393http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/21481393
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http://purl.uniprot.org/uniprot/Q61009#attribution-4B9AA4F814CFD10882C7AA4755C74F77http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/21481393
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http://purl.uniprot.org/uniprot/#_D3Z5U8-mappedCitation-21481393http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21481393
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