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Papers In Press, published online ahead of print October 16, 2003
J. Lipid Res., doi:10.1194/jlr.M300319-JLR200
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Department of Internal Medicine, University of Kentucky, Lexington, KY 42536-0084
Corresponding Author: nrwebb1{at}uky.edu
The class B scavenger receptor BI (SR-BI) recognizes a broad variety of lipoprotein ligands, including HDL, LDL and oxidized LDL. In this study, we investigated whether SR-BI plays a role in the metabolism of cholesterol-rich lipoprotein remnants that accumulate in apoE-/- mice. These particles have an unusual apolipoprotein composition compared to conventional VLDL and LDL, containing mostly apoB-48 as well as substantial amounts of apoA-I and apoA-IV. To study SR-BI activity in vivo, the receptor was over-expressed in apoE-/- mice by adenoviral vector-mediated gene transfer. An ~10-fold increase in liver SR-BI expression resulted in no detectable alterations in VLDL-sized particles, and a modest depletion of cholesterol in IDL-LDL sized lipoprotein particles. This decrease was not due to altered secretion of apoB-containing lipoproteins in SR-BI over-expressing mice. To directly assess whether SR-BI metabolizes apoE-/- mouse lipoprotein remnants, in vitro assays were performed in both CHO cells and primary hepatocytes expressing high levels of SR-BI. This analysis showed a remarkable deficiency of these particles to serve as substrates for selective lipid uptake, despite high affinity, high capacity binding to SR-BI. Taken together, these data establish that SR-BI does not play a direct role in the metabolism of apoE-/- mouse lipoprotein remnants.s
Revised on September 29, 2003
Accepted on October 15, 2003
ApoB-containing lipoproteins in apoE-deficient mice are not metabolized by the class B scavenger receptor BI
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