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Apolipoprotein CI inhibits scavenger receptor BI and increases plasma HDL levels in vivo

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Author: Haan, W. de · Out, R. · Berbée, J.F.P. · Hoogt, C.C. van der · Dijk, K.W.v. · Berkel, T.J.C. van · Romijn, J.A. · Wouter Jukema, J. · Havekes, L.M. · Rensen, P.C.N.
Institution: TNO Kwaliteit van Leven
Source:Biochemical and Biophysical Research Communications, 4, 377, 1294-1298
Identifier: 241309
doi: doi:10.1016/j.bbrc.2008.10.147
Keywords: Health · Physiological Sciences · High density lipoprotein · Oxidized LDL · SR-BI · Transgenic mice · cholesterol ester · high density lipoprotein cholesterol · scavenger receptor BI · Adenovirus · animal cell · cholesterol metabolism · dose response · in vivo study · liver cell · mouse · nonhuman · particle size · protein expression · Adenoviridae · Animals · Apolipoprotein C-I · Cholesterol, HDL · Gene Transfer Techniques · Hepatocytes · Humans · Mice · Mice, Knockout · Scavenger Receptors, Class B · Adenoviridae · Murinae · Mus · Mus musculus


Apolipoprotein CI (apoCI) has been suggested to influence HDL metabolism by activation of LCAT and inhibition of HL and CETP. However, the effect of apoCI on scavenger receptor BI (SR-BI)-mediated uptake of HDL-cholesteryl esters (CE), as well as the net effect of apoCI on HDL metabolism in vivo is unknown. Therefore, we evaluated the effect of apoCI on the SR-BI-mediated uptake of HDL-CE in vitro and determined the net effect of apoCI on HDL metabolism in mice. Enrichment of HDL with apoCI dose-dependently decreased the SR-BI-dependent association of [3H]CE-labeled HDL with primary murine hepatocytes, similar to the established SR-BI-inhibitors apoCIII and oxLDL. ApoCI deficiency in mice gene dose-dependently decreased HDL-cholesterol levels. Adenovirus-mediated expression of human apoCI in mice increased HDL levels at a low dose and increased the HDL particle size at higher doses. We conclude that apoCI is a novel inhibitor of SR-BI in vitro and increases HDL levels in vivo. © 2008 Elsevier Inc. All rights reserved.