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A more recent version of this article appeared on January 1, 2006

Papers In Press, published online ahead of print October 7, 2005
J. Lipid Res., doi:10.1194/jlr.M500255-JLR200
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Submitted on June 17, 2005
Revised on September 27, 2005
Accepted on October 7, 2005

Reevaluation of the role of the multidrug resistant P-glycoprotein in cellular cholesterol homeostasis

Wilfried Le Goff, Megan Settle, Diane J. Greene, Richard E. Morton, and Jonathan D. Smith

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

Corresponding Author: smithj4{at}ccf.org

The multidrug resistance P-glycoprotein (P-gp) was recently proposed to redistribute cholesterol in plasma membrane, thus suggesting that P-gp could modulate cholesterol efflux to cholesterol acceptors. To address this hypothesis and in order to reevaluate the role of P-gp in cholesterol homeostasis, we first analyzed the role of the P-gp expression on cholesterol efflux in P-gp stably-transfected drug-selected LLC-MDR1 cells. Cholesterol efflux to methyl-beta -cyclodextrin (CD) was 4-fold higher in LLC-MDR1 cells as compared to control LLC-PK1 cells, indicating that the accessible pool of plasma membrane cholesterol was increased by P-gp expression. However using P-gp inducible cells lines, HeLa MDR-Tet and 77.1 MDR-Tet, cholesterol efflux to CD, apolipoprotein A-I, or high density lipoproteins (HDL) was not associated with P-gp expression. In addition, we did not observe any effect of P-gp expression on cellular free and esterified cholesterol content, cholesteryl ester uptake from low density lipoproteins and HDL particles, or acyl-coenzyme A: cholesterol acyltransferase activity. We therefore conclude that P-gp expression does not play a major role in cholesterol homeostasis in P-gp inducible cells and that effects of P-gp on cholesterol homeostasis previously described in drug-selected cells might result from non-P-gp pathways that were also induced by selection for drug resistance.


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