J. Lipid Res.
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A more recent version of this article appeared on June 1, 2003

Papers In Press, published online ahead of print April 1, 2003
J. Lipid Res., doi:10.1194/jlr.M200464-JLR200
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Submitted on December 11, 2002
Revised on March 17, 2003
Accepted on March 27, 2003

Cyclodextrins of high and low cholesterol affinity differentially mobilize free and esterified cholesterol from primary human foam cell macrophages

Sue M. Liu, Anne Cogny, Maaike Kockx, Roger T. Dean, Katharina Gaus, Wendy Jessup, and Leonard Kritharides

Macrophage Biology Group, Centre for Thrombosis and Vascular Research, Sydney, NSW 2052

Corresponding Author: l.kritharides{at}unsw.edu.au

Human monocyte-derived macrophage foam cells (HMFC) are resistant to cholesterol efflux mediated by physiological acceptors. The role of the plasma membrane in regulating depletion of free cholesterol (FC) and of cholesteryl ester (CE) was investigated using cyclodextrins (CDs). HMFC were incubated in media containing CDs (1.0 mg/ml, ?0.7mM) with low (hydroxypropyl-beta CD, HP-CD) or high (trimethyl-beta CD, TM-CD) affinity for cholesterol, in the presence or absence of phospholipid vesicles (PLV). Low affinity HP-CD caused minimal cholesterol efflux on its own, but HP-CD+PLV depleted cell FC and CE to 54.5±6.7% of control by 24h. TM-CD depleted FC at least as well as HP-CD+PLV but without depleting CE, even when combined with PLV. This was not explained by acceptor saturation, instability of PLV vesicles, de novo cholesterol synthesis, kinetically distinct cholesterol pools, or inhibition of CE hydrolysis. TM-CD did, however, deplete CE when lower concentrations of TM-CD were combined with PLV, and when acetyl-CoA cholesteryl acyl transferase (ACAT) was inhibited. TM-CD caused much greater depletion of plasma membrane cholesterol than HP-CD without depleting plasma membrane sphingomyelin. It is concluded that differential depletion of plasma membrane cholesterol pools regulates cholesterol efflux and CE clearance in human macrophages.


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