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Originally published In Press as doi:10.1194/jlr.M600259-JLR200 on November 1, 2006

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Journal of Lipid Research, Vol. 48, 366-372, February 2007
Copyright © 2007 by American Society for Biochemistry and Molecular Biology

Regulation of macrophage apoE secretion and sterol efflux by the LDL receptor

Danijela Lucic*, Zhi Hua Huang*, De Sheng Gu*, Michael K. Altenburg{dagger}, Nobuyo Maeda{dagger} and Theodore Mazzone1,§

* Department of Medicine, University of Illinois at Chicago, Chicago, IL
{dagger} Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC
§ Departments of Medicine and Pharmacology, University of Illinois at Chicago, Chicago, IL

Published, JLR Papers in Press, November 1, 2006.

1 To whom correspondence should be addressed. e-mail: tmazzone{at}uic.edu

Factors that regulate apolipoprotein E (apoE) secretion by macrophages will have important effects on vessel wall lipid flux and atherosclerosis. Macrophages express the LDL receptor, which binds apoE with high affinity and could thereby affect the net secretion of apoE from macrophages. In these studies, we demonstrate that treatment of J774 macrophages transfected to constitutively express a human apoE3 cDNA with simvastatin, to increase LDL receptor activity, reduces the secretion of apoE. To further examine the relationship between LDL receptor expression and apoE secretion from macrophages, mouse peritoneal macrophages (MPMs) were isolated from mice with constitutively high expression of human LDL receptor to increase overall LDL receptor expression by 2- to 3-fold. Cells with increased LDL receptor expression also showed reduced apoE secretion compared with MPMs with basal LDL receptor expression. The effect of changes in LDL receptor expression on apoE secretion was isoform-specific, with greater reduction of apoE4 compared with apoE3 secretion and no reduction of apoE2 secretion, paralleling the known affinity of each isoform for LDL receptor binding. The effect of the LDL receptor on apoE secretion for each isoform was further reflected in LDL receptor-dependent changes in apoE-mediated cholesterol efflux. These results establish a regulatory interaction between two branches of macrophage sterol homeostatic pathways that could facilitate a rapid response to changes in macrophage sterol content relative to need.

Supplementary key words atherosclerosis • apolipoproteins • lipoprotein receptors • low density lipoprotein • apolipoprotein E

Abbreviations: apoE, apolipoprotein E; Ldlr, macrophages with increased low density lipoprotein receptor expression; MPM, mouse peritoneal macrophage; WT, macrophages with basal low density lipoprotein expression


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