Factors Influencing the Ability of HDL to Inhibit Expression of Vascular Cell Adhesion Molecule-1 in Endothelial Cells

From the University of Adelaide, Department of Medicine, Royal Adelaide Hospital (D.T.A., M.A.C., P.J.B.), the Cardiovascular Investigation Unit, Royal Adelaide Hospital (K.A.-R.), and the Hanson Centre for Cancer Research, Department of Human Immunology, IMVS (M.A.V., J.R.G.), Adelaide, South Australia, Australia.

Correspondence to Professor Philip J. Barter MBBS, PhD, Department of Medicine, Royal Adelaide Hospital, North Terrace, Adelaide, South Australia, Australia 5000.

Abstract—We have previously reported that high density lipoproteins (HDLs) inhibit the cytokine-induced expression of adhesion molecules in endothelial cells. Here we investigate whether different preparations of HDLs vary in their ability to inhibit the expression of vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells (HUVECs) activated by tumor necrosis factor- (TNF-). HDLs collected from a number of different human subjects all inhibited VCAM-1 expression in a concentration-dependent manner, although the extent of inhibition varied widely between subjects. The inhibitory activities of the HDL₂ and HDL₃ subfractions isolated from individual subjects also differed. Whether equated for concentrations of apolipoprotein (apo) A-I or cholesterol, the inhibitory activity of HDL₃ was superior to that of HDL₂. This difference remained apparent even when the HDL subfractions were present only during preincubations with the HUVECs and were removed before activation by TNF-. To determine whether the inhibitory effect of HDL₃ was influenced by apolipoprotein composition, preparations of HDL₃ were modified by replacing all of their apo A-I with apo A-II. This change in apolipoprotein composition had no effect on the ability of the HDL₃ to inhibit endothelial VCAM-1 expression. Thus, it has been shown that different preparations of HDLs differ markedly in their abilities to inhibit VCAM-1 expression in cytokine-activated HUVECs. The mechanism underlying the differences remains to be determined.

Key Words: endothelial cells • vascular cell adhesion molecule-1 • HDL • HDL subfractions • atherosclerosis

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