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Papers In Press, published online ahead of print August 10, 2006
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Medicine, University of Washington, Seattle, WA 98195-6426
Corresponding Author: smashie{at}u.washington.edu
Recent developments in lipid metabolism have shown the importance of ATP binding cassette transporters (ABCs) in controlling cellular and total body lipid homeostasis. ABCA1 mediates the transport of cholesterol and phospholipids from cells to lipid-poor apolipoprotein A-I (apoA-I), whereas ABCG1 and ABCG4 mediate the transport of cholesterol from cells to lipidated lipoproteins. ABCA1, ABCG1, and ABCG4 are all expressed in cholesterol-loaded macrophages, and macrophages from ABCA1 and ABCG1 knockout mice accumulate cholesteryl esters. Here we show that the lipidated particles generated by incubating cells over-expressing ABCA1 with apoA-I are efficient acceptors for cholesterol released from cells over-expressing either ABCG1 or ABCG4. The cholesterol released to the particles were derived from a cholesterol oxidase-accessible plasma membrane pool in both the ABCG1 and ABCG4 cells, which is the same pool of cholesterol previously shown to be removed by high density lipoproteins. ABCA1 cells incubated with apoA-I generated two major populations of cholesterol- and phospholipid-rich lipoprotein particles that were converted by ABCG1 or ABCG4 cells to one major particle population that was highly enriched in cholesterol. The results suggest that ABCG1 and ABCG4 act in concert with ABCA1 to maximize the removal of excess cholesterol from cells and to generate cholesterol-rich lipoprotein particles.
Revised on August 4, 2006
Accepted on August 10, 2006
ABCA1 and ABCG1 or ABCG4 act sequentially to remove cellular cholesterol and generate cholesterol-rich HDL
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