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Papers In Press, published online ahead of print March 1, 2003
J. Lipid Res., doi:10.1194/jlr.M200273-JLR200
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Cardiology, McGill University Health Centre, Montreal, QC H3A 1A1
Corresponding Author: michel.marcil{at}mcgill.ca
Recent evidence from in vitro studies suggests that minimally lipidated apoE has direct cell regulatory functions that are protective against vascular disease. To investigate the metabolism of such apoE-containing particles in human plasma, we isolated a fraction of plasma HDL-apoE particles that lack apolipoprotein A-I (HDL-LpE) from subjects with apoE3/3 phenotype by immunoaffinity. Plasma HDL-LpE had a particle size ranging from 9 to 18.5 nm in diameter and was characterized by two dimensional gel (2D-PAGGE) as having either
Revised on February 19, 2003
Accepted on February 25, 2003
Structural and functional properties of human plasma high density-sized lipoprotein containing only apoE particles (HDL-LpE)
-, pre
1-, pre2- or 
-electrophoretic mobility. HDL-LpE particles were also present in the medium of cultured human hepatoma cell lines (HepG2) and monocyte-derived macrophages. The majority of apoE3 was found as a monomeric form in HDL-LpE particles. Most of the plasma HDL-LpE floated at d > 1.21 g/mL. Plasma levels of HDL-LpE in normolipidemic, CETP deficient and ABCA1 deficient subjects were 0.72±0.15 mg/dL (n=12), 1.77±0.75 mg/dL (n=3) and 0.55±0.11 mg/dL (n=3), respectively. The ratio of HDL-apoE containing apoA-I to HDL-LpE was significantly higher 4h after a fat load, representing a 35±9% increase (n=3) compared to the fasting state (0 h). Immunoaffinity isolated plasma HDL-LpE3 particles were as effective as apoE3, reconstituted HDL particles r(LpE3) or apoA-I in promoting efflux of acetyl-LDL-derived [3H]-cholesterol from J744 macrophages. These results demonstrate that: (1) plasma HDL-LpE particles may have hepatogenous and macrophagic origins; (2) HDL-LpE particles were preserved even with large reductions in apoA-I-containing lipoproteins; (3) HDL-LpE particles were active in the transfer of apoE to triglyceride-rich lipoproteins (TRL); and (4) HDL-LpE efficiently take up cell-derived cholesterol.
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