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Updated: Jul 14, 2026

Quantitation of Endothelial Cell Adhesiveness In Vitro
Published on: June 18, 2015
Endothelial and leukocyte adhesion molecules in primary hypertriglyceridemia
María Belén Benítez1, Luis Cuniberti, María Cecilia Fornari
1Laboratory of Lipids and Lipoprotein, Department of Clinical Biochemistry, Faculty of Pharmacy and Biochemistry, University of Buenos Aires, Junin 956, Buenos Aires 1113, Argentina.
Primary hypertriglyceridemia elevates key inflammatory markers, including soluble VCAM-1 and ICAM-1, and leukocyte-associated CD18 and CD54. These findings highlight the inflammatory process contributing to atherosclerosis development in these patients.
Area of Science:
- Cardiovascular Biology
- Immunology
- Metabolic Disorders
Background:
- Hypertriglyceridemia impairs endothelial function, increasing atherosclerosis risk.
- Key steps in atherosclerotic plaque development in primary hypertriglyceridemia remain unclear.
Purpose of the Study:
- To investigate soluble and leukocyte-associated cell adhesion molecule expression in primary hypertriglyceridemia.
- To compare these markers in patients with and without metabolic syndrome against controls.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) and flow cytometry were used.
- Measured soluble VCAM-1, ICAM-1, E-selectin, and leukocyte CD18, CD49d, CD54.
- Analyzed lipid profiles, CETP activity, HDL, and VLDL composition.
Main Results:
- Significantly elevated VCAM-1 and ICAM-1 in hypertriglyceridemic patients versus controls.
- Increased monocyte CD18, CD54, and lymphocyte CD18 in hypertriglyceridemic patients.
- Elevated ICAM-1, monocyte CD18/CD54, and lymphocyte CD18 persisted even after excluding metabolic syndrome.
Conclusions:
- Elevated circulating and leukocyte adhesion molecules indicate an inflammatory process in primary hypertriglyceridemia.
- This inflammation is a critical factor in the pathogenesis of atherosclerosis.
- Adhesion molecules may serve as biomarkers for early atherosclerotic changes in hypertriglyceridemia.
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