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A more recent version of this article appeared on November 1, 2004

Papers In Press, published online ahead of print August 16, 2004
J. Lipid Res., doi:10.1194/jlr.M400191-JLR200
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Submitted on May 21, 2004
Revised on August 2, 2004
Accepted on August 6, 2004

Quantitative analysis in scavenger-receptor BI (SR-BI) knock-out mice indicates the essential role of SR-BI in the selective uptake of cholesteryl esters from HDL by the liver and the adrenals

Ruud Out, Menno Hoekstra, John A. A. Spijkers, Johan K. Kruijt, Miranda Van Eck, Ingrid S. T. Bos, Jaap Twisk, and Theo J. C. Van Berkel

Leiden University, Division of Biopharmaceutics,LACDR, Leiden 2300 RA

Corresponding Author: t.berkel{at}lacdr.leidenuniv.nl

Scavenger receptor BI (SR-BI) has been identified as a functional high-density lipoprotein (HDL) binding protein which can mediate the selective uptake of cholesteryl esters (CE) from HDL. To quantify the in vivo role of SR-BI in the process of selective uptake, HDL was labeled with cholesteryl ether ([3H]CEt-HDL) and 125I-tyramine cellobiose ([125I]-TC-HDL), and injected into SR-BI knock-out (KO) and wild-type (WT) mice. In SR-BI KO mice, the clearance of HDL-CE from the blood circulation is greatly diminished (0.0430.004 pools/h for SR-BI KO mice vs. 0.1060.004 pools/h for WT mice) while the liver and adrenal uptake is greatly lowered. Utilization of double labeled HDL ([3H]Cet and [125I]-TC) indicated the total absence in vivo of the selective decay and liver uptake of CE from HDL in SR-BI KO mice. Parenchymal cells isolated from SI-BI KO mice showed similar association values for [3H]Cet and [125I]TC in contrast with WT cells, indicating that in parenchymal liver cells SR-BI is the only molecule exerting selective CE uptake from HDL. Thus, in vivo and in vitro, SR-BI is the sole molecule mediating the selective uptake of CE from HDL by the liver and the adrenals, making it the unique target to modulate reverse cholesterol transport.


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