HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: M700200-JLR200v1 49/1/107    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Yvan-Charvet, L. Articles by Tall, A. R. Search for Related Content PubMed PubMed Citation Articles by Yvan-Charvet, L. Articles by Tall, A. R. Social Bookmarking                      What's this?

Journal of Lipid Research, Vol. 49, 107-114, January 2008
Copyright © 2008 by American Society for Biochemistry and Molecular Biology

SR-BI inhibits ABCG1-stimulated net cholesterol efflux from cells to plasma HDL

Laurent Yvan-Charvet^1,*, Tamara A. Pagler^*, Nan Wang^*, Takafumi Senokuchi^*, May Brundert, Hongna Li^*, Franz Rinninger and Alan R. Tall^*

^* Division of Molecular Medicine, Department of Medicine, Columbia University, New York, NY
University Hospital Hamburg Eppendorf, Hamburg, Germany

Published, JLR Papers in Press, October 24, 2007.

¹ To whom correspondence should be addressed. e-mail: ly2159{at}columbia.edu

This study compares the roles of ABCG1 and scavenger receptor class B type I (SR-BI) singly or together in promoting net cellular cholesterol efflux to plasma HDL containing active LCAT. In transfected cells, SR-BI promoted free cholesterol efflux to HDL, but this was offset by an increased uptake of HDL cholesteryl ester (CE) into cells, resulting in no net efflux. Coexpression of SR-BI with ABCG1 inhibited the ABCG1-mediated net cholesterol efflux to HDL, apparently by promoting the reuptake of CE from medium. However, ABCG1-mediated cholesterol efflux was not altered in cholesterol-loaded, SR-BI-deficient (SR-BI^–/–) macrophages. Briefly cultured macrophages collected from SR-BI^–/– mice loaded with acetylated LDL in the peritoneal cavity did exhibit reduced efflux to HDL. However, this was attributable to reduced expression of ABCG1 and ABCA1, likely reflecting increased macrophage cholesterol efflux to apolipoprotein E-enriched HDL during loading in SR-BI^–/– mice. In conclusion, cellular SR-BI does not promote net cholesterol efflux from cells to plasma HDL containing active LCAT as a result of the reuptake of HDL-CE into cells. Previous findings of increased atherosclerosis in mice transplanted with SR-BI^–/– bone marrow probably cannot be explained by a defect in macrophage cholesterol efflux.

Supplementary key words high density lipoprotein • ATP binding cassette transporter G1 • scavenger receptor class B type I • lecithin:cholesterol acyltransferase • liver X receptor • macrophage

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				N. Mukhamedova, G. Escher, W. D'Souza, U. Tchoua, A. Grant, Z. Krozowski, M. Bukrinsky, and D. Sviridov Enhancing apolipoprotein A-I-dependent cholesterol efflux elevates cholesterol export from macrophages in vivo J. Lipid Res., November 1, 2008; 49(11): 2312 - 2322. [Abstract] [Full Text] [PDF]