J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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A more recent version of this article appeared on July 1, 2005 Originally published In Press as doi:10.1194/jlr.M400477-JLR200 on January 16, 2005

Papers In Press, published online ahead of print May 31, 2005
J. Lipid Res., doi:10.1194/jlr.M400477-JLR200
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Submitted on December 6, 2004
Revised on January 1, 1998
Accepted on January 4, 2005

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 Genest

Cardiology Dept., McGill University Health Center, Montreal, QC H3A 1A1

Corresponding Author: jacques.genest{at}muhc.mcgill.ca

It has been suggested that ABCA1 interacts preferentially with lipid-poor apoA-I. Here, we show that treatment of plasma with dimyristoyl phosphatidylcholine multilamellar vesicles (DMPC-MLV) generates pre-beta 1-LpA-I-like particles similar to those of native plasma. Isolated pre-beta 1-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 mu g/mL). We next investigated the ability of pre-beta 1-LpA-I-like particles to promote cholesterol efflux from J774 macrophages stimulated or not with cAMP. DMPC enrichment of plasma promoted cholesterol efflux from either stimulated or unstimulated cells in a dose-dependent manner. Comparison of maximal efflux (Vmax efflux) and the DMPC concentration that elicited half maximal efflux (EC50 efflux) between unstimulated and stimulated cells after a 4-hour incubation showed that Vmax efflux is significantly higher for stimulated cells (11.8 ± 1.2 % vs. 8.7 ± 0.5 %), whereas the value of EC50 efflux is higher for unstimulated cells (610 ± 89 vs. 136 ± 16 µM DMPC). Furthermore, cholesterol efflux to DMPC-treated plasma was reduced by 30% in the presence of glyburide. Finally, treatment of Tangier disease (TD) plasma with DMPC affected neither the amount of pre-beta -HDL nor cholesterol efflux. These results indicate that DMPC enrichment of normal plasma resulted in redistribution of apoA-I from &alpha -HDL to pre-beta -HDL, allowing for more efficient ABCA1-mediated cholesterol release. Increasing plasma prebeta 1-LpA-I level by either pharmacological agents or direct infusions might prevent foam cell formation and reduce atherosclerotic vascular disease.


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