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Elevated soluble cellular adhesion molecules in subjects with low HDL-cholesterol
Laura Calabresi1, Monica Gomaraschi, Barbara Villa
1Center E. Grossi Paoletti, Department of Pharmacological Sciences, University of Milano, Italy.
Arteriosclerosis, Thrombosis, and Vascular Biology
|April 16, 2002
Summary
Low HDL cholesterol is linked to higher levels of cellular adhesion molecules (CAMs), specifically sICAM-1 and sE-selectin. This suggests a mechanism where low HDL may promote atherosclerosis and related events.
Area of Science:
- Cardiovascular Science
- Biochemistry
- Immunology
Background:
- Low levels of high-density lipoprotein cholesterol (HDL-C) are associated with increased cardiovascular risk.
- Cellular adhesion molecules (CAMs) play a role in atherogenesis and inflammatory processes.
Purpose of the Study:
- To investigate if cellular adhesion molecule (CAM) expression is elevated in individuals with low HDL cholesterol.
- To explore the relationship between HDL-C levels and plasma concentrations of soluble vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1), and E-selectin (sE-selectin).
Main Methods:
- Measured plasma levels of sVCAM-1, sICAM-1, and sE-selectin in subjects categorized by HDL-C levels (low, average, high).
- Analyzed correlations between HDL-C and CAM levels.
- Assessed the impact of fenofibrate-induced HDL-C increase on CAM concentrations in low-HDL subjects.
Main Results:
- Significantly higher average levels of sICAM-1 and sE-selectin were observed in individuals with low HDL-C compared to those with average or high HDL-C.
- Plasma sVCAM-1 concentrations did not show significant differences across HDL-C groups.
- HDL-C was inversely correlated with sICAM-1 and sE-selectin in low-HDL subjects.
- Fenofibrate treatment led to a significant reduction in sICAM-1 and sE-selectin levels as HDL-C increased.
Conclusions:
- Increased expression of CAMs, specifically sICAM-1 and sE-selectin, is associated with low HDL-C levels.
- Elevated CAM expression may represent a mechanism through which low HDL-C contributes to atherogenesis and acute atherothrombotic events.