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J Biol Chem, Vol. 273, Issue 14, 8434-8438, April 3, 1998

In Vivo Regulation of Scavenger Receptor BI and the Selective Uptake of High Density Lipoprotein Cholesteryl Esters in Rat Liver Parenchymal and Kupffer Cells

Kees Fluiter, Deneys R. van der Westhuijzen^§, and Theo J. C. van Berkel

From the  Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, University of Leiden, Sylvius Laboratories, P. O. Box 9503, 2300 RA Leiden, The Netherlands and the ^§ Department of Internal Medicine, University of Kentucky Medical Center, Lexington, Kentucky 40536-0284

High density lipoprotein cholesteryl esters (HDL-CE) are selectively taken up by liver parenchymal cells without parallel apolipoprotein uptake. This selective uptake route forms an important step in the so-called reverse cholesterol transport. Scavenger receptor BI (SR-BI) is the only known HDL receptor which can mediate selective uptake of HDL-CE. In the present study we investigated its regulation in liver cells. The down-regulation of SR-BI expression in liver by 17-ethinyl estradiol (EE) treatment was found by immunoblotting to be the consequence of down-regulation of SR-BI in parenchymal cells, while SR-BI expression in Kupffer cells was up-regulated. The selective uptake of HDL-CE in vivo by parenchymal and Kupffer cells was measured by labeling of HDL with [³H]CE and analysis of the cellular uptake at 10 min after injection. After EE treatment, uptake of [³H]CE-labeled HDL by parenchymal cells decreased by 85%, while Kupffer cells showed a 4-fold increase in selective uptake of [³H]CE-labeled HDL. In vitro studies with isolated parenchymal cells indicated that after EE treatment, the selective uptake of [³H]CE labeled HDL was 3-4-fold lower, indicating that the in vivo observations are also reflected in vitro. A 2-week high-cholesterol diet leads to lowering of SR-BI expression in parenchymal cells, while the expression in Kupffer cells is increased. Like EE treatment, the selective uptake of [³H]CE-labeled HDL by the two hepatic cell types in vivo correlated with the changes in expression of SR-BI. Our results thus demonstrate that within the liver, the regulation of SR-BI expression by EE treatment or a high-cholesterol diet, correlates with changes in the selective uptake of HDL-CE, supporting a function of SR-BI to mediate the selective uptake of HDL-CE in the liver parenchymal cells. The contrasting regulatory effect on parenchymal cells and Kupffer cells might indicate a different function of SR-BI in the latter cell type.

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Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.

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