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A more recent version of this article appeared on October 1, 2005

Papers In Press, published online ahead of print July 16, 2005
J. Lipid Res., doi:10.1194/jlr.M500059-JLR200
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Submitted on February 16, 2005
Revised on June 17, 2005
Accepted on July 6, 2005

Aggregated LDL and lipid dispersions induce lysosomal cholesteryl ester accumulation in macrophage foam cells

Evelyn E. Griffin, Jody C. Ullery, Brian E. Cox, and W. Gray Jerome

Pathology Dept., Vanderbilt University School of Medicine, Nashville, TN 37232-2561

Corresponding Author: jay.jerome{at}vanderbilt.edu

Macrophage foam cells in atherosclerotic lesions accumulate substantial cholesterol stores within large, swollen lysosomes. Previous studies with mildly oxidized low density lipoprotein (oxLDL)-treated THP-1 macrophages suggest an initial build up of free cholesterol (FC), followed by an inhibition of lysosomal cholesteryl ester (CE) hydrolysis and a subsequent lysosomal accumulation of unhydrolyzed lipoprotein CE. We examined whether other potential sources of cholesterol found within atherosclerotic lesions could also induce similar lysosomal accumulation. Biochemical analysis combined with microscopic analysis showed that treatment of THP-1 macrophages with aggregated (agg)LDL or CE-rich lipid dispersions (DISP) produced a similar lysosomal accumulation of both FC and CE. Co-treatment with an ACAT inhibitor, CP113,818, confirmed that the CE accumulation was primarily the result of inhibition of lysosomal CE hydrolysis. The rate of unhydrolyzed CE build up was more rapid with DISP compared to that with aggLDL. However, with both treatments, FC appeared to accumulate in lysosomes prior to inhibition in hydrolysis and CE accumulation, a sequence shared with mildly oxLDL. Thus, lysosomal accumulation of FC and CE can be due to more general mechanisms than just inhibition of hydrolysis by oxidized lipids.


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P. G. Yancey, W. G. Jerome, H. Yu, E. E. Griffin, B. E. Cox, V. R. Babaev, S. Fazio, and M. F. Linton
Severely altered cholesterol homeostasis in macrophages lacking apoE and SR-BI
J. Lipid Res., May 1, 2007; 48(5): 1140 - 1149.
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