Apolipoprotein CI inhibits scavenger receptor BI and increases plasma HDL levels in vivo
article
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.
Topics
Physiological SciencesHigh density lipoproteinOxidized LDLSR-BITransgenic micecholesterol esterhigh density lipoprotein cholesterolscavenger receptor BIAdenovirusanimal cellcholesterol metabolismdose responsein vivo studyliver cellmousenonhumanparticle sizeprotein expressionAdenoviridaeAnimalsApolipoprotein C-ICholesterol, HDLGene Transfer TechniquesHepatocytesHumansMiceMice, KnockoutScavenger Receptors, Class BAdenoviridaeMurinaeMusMus musculus
TNO Identifier
241309
ISSN
0006291X
Source
Biochemical and Biophysical Research Communications, 377(4), pp. 1294-1298.
Pages
1294-1298
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