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A more recent version of this article appeared on April 1, 2004

Papers In Press, published online ahead of print January 1, 2004
J. Lipid Res., doi:10.1194/jlr.M300336-JLR200
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Submitted on July 30, 2003
Revised on December 23, 2003
Accepted on December 24, 2003

ABCA1 mediates concurrent cholesterol and phospholipid efflux to apoAI

Jonathan D. Smith, Wilfried Le Goff, Megan Settle, Gregory Brubaker, Christine Waelde, Andrew Horwitz, and Michael N. Oda

Department of Cell Biology, NC10, Cleveland Clinic Foundation, Cleveland, OH 44195

Corresponding Author: smithj{at}lerner.ccf.org

Prior studies provide data supporting that ABCA1 promotes lipid efflux to extracellular acceptors in a two-step fashion; first, ABCA1 mediates phospholipid efflux to an apolipoprotein, and second, this apolipoprotein-phospholipid complex accepts free cholesterol in an ABCA1-independent fashion. In the current study using RAW264.7 cells, ABCA1-mediated free cholesterol and phospholipid efflux to apoAI were tightly coupled to each other both temporally and after treatment with ABCA1 inhibitors. The time course and temperature dependence of ABCA1-mediated lipid efflux to apoAI support of a role for endocytosis in this process. Cyclodextrin treatment of RAW264.7 cells partially inhibited 8Br-cAMP induced efflux of free cholesterol and phospholipid to apoAI. ABCA1 expressing cells are more sensitive to cell damage by high dose cyclodextrin and vanadate, leading to increased lactate dehydrogenase leakage and phospholipid release even in the absence of the acceptor apoAI. Finally, we could not reproduce a two-step effect on lipid efflux using conditioned media from ABCA1 expressing cells pretreated with cyclodextrin.


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