Atherosclerosis and Lipoproteins |
From the Center E. Grossi Paoletti, Department of Pharmacological Sciences, University of Milano, Italy.
Address correspondence to Prof. Guido Franceschini, Center E. Grossi Paoletti, Department of Pharmacological Sciences, Via Balzaretti 9, 20133 Milano, Italy. E-mail Guido.Franceschini{at}unimi.it
The purpose of this study was to investigate whether the expression of cellular adhesion molecules (CAMs) is enhanced in individuals with low HDL cholesterol (HDL-C). Plasma levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1), and E-selectin (sE-selectin) were measured in subjects with low (below the 10th percentile for the Italian population), average, or high (above the 90th percentile) HDL-C. Average sICAM-1 and sE-selectin levels were significantly higher in two groups of 65 individuals with low HDL levels, either hyperlipidemic (320.5±16.0 and 61.4±3.5 ng/mL) or normolipidemic (309.6±13.0 and 60.0±2.7 ng/mL), than in subjects with average HDL levels, either hyperlipidemic (267.0±10.1 and 50.4±2.8 ng/mL) or normolipidemic (257.9±5.4 and 51.1±2.4 ng/mL), or with high HDL levels (254.8±10.2 and 52.5±3.2 ng/mL). No significant difference was found in the plasma sVCAM-1 concentration. HDL-C was inversely correlated with sICAM-1 and sE-selectin in the low-HDL subjects (r2=0.087 and 0.035, P=0.0007 and 0.033, respectively), but not in individuals with normal or elevated HDL-C (r2=0.012 and 0.006). A fenofibrate-induced increase of HDL-C in 20 low-HDL subjects was associated with a significant reduction of plasma sICAM-1 and sE-selectin concentrations. An increased CAMs expression may be a mechanism by which a low plasma HDL level promotes atherogenesis and causes acute atherothrombotic events.
Key Words: HDL intracellular adhesion molecule-1 E-selectin vascular cell adhesion molecule-1 atherosclerosis
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