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J. Biol. Chem., Vol. 276, Issue 47, 43564-43569, November 23, 2001
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From the Division of Molecular Medicine, Department of Medicine,
Columbia University, New York, New York 10032
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 low density lipoprotein
(where cholesterol accumulates in late endosomes and lysosomes)
compared with cells labeled with [3H]cholesterol with
10% fetal bovine serum, 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 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
Niemann-Pick C1 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.
Preferential ATP-binding Cassette Transporter A1-mediated
Cholesterol Efflux from Late Endosomes/Lysosomes*
,,
*
This work was supported by Specialized Center of Research in
Atherosclerosis Grant HL-56984 (to A. R. T. and I. T) from
the NHLBI, National Institutes of Health, and research grants from the
Parshegian Foundation (to A. R. T) and Berlex Biosciences (to
I. T.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
These authors made equal contributions to the work.
§
To whom correspondence should be addressed: Div. of Molecular
Medicine, Dept. of Medicine, Columbia University, 603 W. 168th St., New York, NY 10032. Tel.: 212-305-9418;
Fax: 212-305-5052; E-mail: art1@columbia.edu.
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