J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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A more recent version of this article appeared on December 1, 2005

Papers In Press, published online ahead of print September 14, 2005
J. Lipid Res., doi:10.1194/jlr.M500263-JLR200
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Submitted on June 21, 2005
Revised on September 1, 2005
Accepted on September 6, 2005

Regulation of selective uptake of cholesteryl esters from the high density lipoproteins by sphingomyelin

Papasani V. Subbaiah, Laurence R. Gesquiere, and Kewei Wang

Medicine Dept., University of Illinois at Chicago, Chicago, IL 60612

Corresponding Author: psubbaia{at}uic.edu

Although sphingomyelin (SM) is a major phospholipid in lipoproteins as well as in the membrane rafts where the scavenger receptor BI (SR-BI) is localized, its possible role in the selective uptake of cholesteryl ester (CE) by the SR-BI-mediated pathway is unknown. We investigated the effect of SM in lipoproteins and cell membranes on the selective uptake in three different cell line: SR-BI-transfected CHO cells, hepatocytes (HepG2), and adrenocortical cells (Y1BS1). Incorporation of SM into recombinant HDL (rHDL) containing labeled CE resulted in up to 50% inhibition of selective uptake of CE in all three cell lines. This inhibition was completely reversed by treatment of rHDL with SMase. Selective uptake from plasma HDL was activated by 22-72% after treatment of HDL with SMase. In addition, pre-treatment of the cells with SMase resulted in stimulation of CE uptake from rHDL by CHO and Y1BS1, although not by HepG2. Incorporation of ceramide into rHDL resulted in upto 2-fold stimulation of CE uptake, although pre-treatment of cells with egg ceramide did not have significant effect. These results show that SM and ceramide in the lipoproteins and the cell membranes regulate the SR-BI-mediated selective uptake of CE, possibly by interacting with the sterol ring or with SR-BI itself.


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