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A more recent version of this article appeared on November 16, 2001
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Papers In Press, published online ahead of print September 14, 2001
J. Biol. Chem, 10.1074/jbc.M107938200
Submitted on August 17, 2001
Revised on September 13, 2001
Accepted on September 14, 2001

Preferential ATP-binding cassette transporter A1 (ABCA1)-mediated cholesterol efflux from late endosomes/lysosomes

Wengen Chen, Yu Sun, Carrie Welch, Anna Gorelik, Andrew R. Leventhal, Ira Tabas, and Alan R. Tall

Division of molecular medicine, Columbia University, New York, NY 10032

Corresponding Author: wc245{at}columbia.edu

Recently, ATP-binding cassette transporter A1 (ABCA1), the defective molecule in Tangier Disease, has been shown to stimulate phospholipid and cholesterol efflux to apolipoprotein A-I (apoA-I); however, little is known concerning the cellular cholesterol pools that act as the source of cholesterol for ABCA1-mediated efflux. We observed a higher level of isotopic and mass cholesterol efflux from mouse peritoneal macrophages labeled with 3H-cholesterol/acetyl-LDL (where cholesterol accumulates in late endosomes and lysosomes), compared to cells labeled with 3H-cholesterol/10% FBS, suggesting that late endosomes/lysosomes act as a preferential source of cholesterol for ABCA1-mediated efflux. Consistent with this idea, macrophages from Niemann-Pick C1 (NPC1) mice (that have an inability to exit cholesterol from late endosomes/lysosomes) showed a profound defect in cholesterol efflux to apoA-I. In contrast, phospholipid efflux to apoA-I was normal in NPC1 macrophages, as was cholesterol efflux following plasma membrane cholesterol labeling. These results suggest that cholesterol deposited in late endosomes/lysosomes preferentially acts as a source of cholesterol for ABCA1-mediated cholesterol efflux.


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