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Journal of Lipid Research, Vol. 48, 348-357, February 2007
Copyright © 2007 by American Society for Biochemistry and Molecular Biology

Dynamics of dense electronegative low density lipoproteins and their preferential association with lipoprotein phospholipase A₂

John W. Gaubatz, Baiba K. Gillard, John B. Massey, Ron C. Hoogeveen, Max Huang, Eric E. Lloyd, Joe L. Raya, Chao-yuh Yang and Henry J. Pownall¹

Section of Atherosclerosis and Lipoprotein Research, Department of Medicine, Baylor College of Medicine, Houston, TX 77030

Published, JLR Papers in Press, November 13, 2006.

¹ To whom correspondence should be addressed. e-mail: hpownall{at}bcm.tmc.edu

Small, dense, electronegative low density lipoprotein [LDL(–)] is increased in patients with familial hypercholesterolemia and diabetes, populations at increased risk for coronary artery disease. It is present to a lesser extent in normolipidemic subjects. The mechanistic link between small, dense LDL(–) and atherogenesis is not known. To begin to address this, we studied the composition and dynamics of small, dense LDL(–) from normolipidemic subjects. NEFA levels, which correlate with triglyceride content, are quantitatively linked to LDL electronegativity. Oxidized LDL is not specific to small, dense LDL(–) or lipoprotein [a] (i.e., abnormal lipoprotein). Apolipoprotein C-III is excluded from the most abundant LDL (i.e., that of intermediate density: 1.034 < d < 1.050 g/ml) but associated with both small and large LDL(–). In contrast, lipoprotein-associated phospholipase A₂ (LpPLA₂) is highly enriched only in small, dense LDL(–). The association of LpPLA₂ with LDL may occur through amphipathic helical domains that are displaced from the LDL surface by contraction of the neutral lipid core.

Supplementary key words atherogenesis • fatty acid • apo B-100

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