J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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A more recent version of this article appeared on June 1, 2005

Papers In Press, published online ahead of print March 16, 2005
J. Lipid Res., doi:10.1194/jlr.M400485-JLR200
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Submitted on December 9, 2004
Revised on March 9, 2005
Accepted on March 10, 2005

Lipoprotein aggregation protects human monocyte-derived macrophages from oxidized LDL-induced cytotoxicity

Reto Asmis, Jim G. Begley, Jennifer Jelk, and William V. Everson

Division of Cardiovascular Medicine, University of Kentucky, Lexington, KY 40436-0200

Corresponding Author: rasmis{at}email.uky.edu

Oxidative modifications render low density lipoprotein cytotoxic and enhance its propensity to aggregate and fuse into particles similar to those found in atherosclerotic lesions. We showed previously that aggregation of oxidized LDL (OxLDL) promotes the transformation of human macrophages into lipid-laden foam cells (Asmis, R. and Jelk, J. Atherosclerosis 2000;148: 243-253). Here we tested the hypothesis that aggregation of OxLDL enhances its clearance by human macrophages and thus may protect macrophages from OxLDL-induced cytotoxicity. We found that increased aggregation of OxLDL correlated with decreased macrophage injury. Using [3H]-labeled and Alexa546-labeled OxLDL, we found that aggregation enhanced OxLDL uptake and increased cholesteryl ester accumulation, but did not alter free cholesterol levels in macrophages. Acetylated LDL was a potent competitor of AggOxLDL uptake suggesting that scavenger receptor A plays an important role in the clearance of AggOxLDL. Inhibitors of actin polymerization cytochalasin B, cytochalasin D and latrunculin A also prevented AggOxLDL uptake and restored OxLDL-induced cytotoxicity. This suggests that OxLDL-induced macrophage injury does not require OxLDL uptake and may occur on the cell surface. Our data demonstrate that aggregation of cytotoxic OxLDL enhances its clearance by macrophages without damage to the cells, thus allowing macrophages to avoid OxLDL-induced cell injury.


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