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Journal of Lipid Research, Vol. 46, 1457-1465, July 2005
Copyright © 2005 by American Society for Biochemistry and Molecular Biology

Structural modification of plasma HDL by phospholipids promotes efficient ABCA1-mediated cholesterol release

Houssein Hajj Hassan, Sacha Blain, Betsie Boucher, Maxime Denis, Larbi Krimbou and Jacques Genest¹

Cardiovascular Genetics Laboratory, Cardiology Division, McGill University Health Center/Royal Victoria Hospital, Montréal, Québec H3A 1A1, Canada

Published, JLR Papers in Press, January 16, 2005. DOI 10.1194/jlr.M400477-JLR200

¹ To whom correspondence should be addressed. e-mail: jacques.genest{at}muhc.mcgill.ca

It has been suggested that ABCA1 interacts preferentially with lipid-poor apolipoprotein A-I (apoA-I). Here, we show that treatment of plasma with dimyristoyl phosphatidylcholine (DMPC) multilamellar vesicles generates preß₁-apoA-I-containing lipoproteins (LpA-I)-like particles similar to those of native plasma. Isolated preß₁-LpA-I-like particles inhibited the binding of ¹²⁵I-apoA-I to ABCA1 more efficiently than HDL₃ (IC₅₀ = 2.20 ± 0.35 vs. 37.60 ± 4.78 µg/ml). We next investigated the ability of DMPC-treated plasma to promote phospholipid and unesterified (free) cholesterol efflux from J774 macrophages stimulated or not with cAMP. At 2 mg DMPC/ml plasma, both phospholipid and free cholesterol efflux were increased (50% and 40%, respectively) in cAMP-stimulated cells compared with unstimulated cells. Similarly, both phospholipid and free cholesterol efflux to either isolated native preß₁-LpA-I and preß₁-LpA-I-like particles were increased significantly in stimulated cells. Furthermore, glyburide significantly inhibited phospholipid and free cholesterol efflux to DMPC-treated plasma. Removal of apoA-I-containing lipoproteins from normolipidemic plasma drastically reduced free cholesterol efflux mediated by DMPC-treated plasma. Finally, treatment of Tangier disease plasma with DMPC affected the amount of neither preß₁-LpA-I nor free cholesterol efflux.

These results indicate that DMPC enrichment of normal plasma resulted in the redistribution of apoA-I from -HDL to preß-HDL, allowing for more efficient ABCA1-mediated cellular lipid release. Increasing the plasma preß₁-LpA-I level by either pharmacological agents or direct infusions might prevent foam cell formation and reduce atherosclerotic vascular disease.

Abbreviations: apoA-I, apolipoprotein A-I; BBSM, bovine brain sphingomyelin; DMPC, dimyristoyl phosphatidylcholine; MLV, multilamellar vesicle; PEG, polyethylene glycol; POPC, palmitoyloleoyl phosphatidylcholine; preß₁-LpA-I, preß₁ apoA-I-containing lipoproteins; RCT, reverse cholesterol transport; SR-BI, scavenger receptor class B type I; TD, Tangier disease; 2D-PAGGE, two-dimensional polyacrylamide nondenaturing gradient gel electrophoresis

Supplementary key words lipid-poor apolipoprotein A-I • ATP binding cassette transporter A1 • cholesterol efflux • high density lipoprotein

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