Related Experiment Videos
Native LDL increases endothelial cell adhesiveness by inducing intercellular adhesion molecule-1
D M Smalley1, J H Lin, M L Curtis
1Department of Experimental Pathology, New York Medical College, Valhalla, NY. USA.
Arteriosclerosis, Thrombosis, and Vascular Biology
|April 1, 1996
Summary
Native low-density lipoprotein (n-LDL) increases endothelial cell adherence by upregulating intercellular adhesion molecule-1 (ICAM-1). This early step in atherogenesis highlights n-LDL
Area of Science:
- Endothelial biology
- Molecular mechanisms of atherosclerosis
- Cellular adhesion
Background:
- Native low-density lipoprotein (n-LDL) is implicated in endothelial dysfunction.
- Endothelial cell (EC) adherence of circulating cells is a key event in vascular inflammation.
Purpose of the Study:
- To investigate the mechanisms by which n-LDL alters endothelial cell adherence.
- To determine the role of cell adhesion molecules in n-LDL-mediated endothelial activation.
Main Methods:
- Human umbilical vein endothelial cells (ECs) were treated with n-LDL.
- U937 cell and primary monocyte/neutrophil adherence assays were performed.
- Intercellular adhesion molecule-1 (ICAM-1), E-selectin, and vascular cell adhesion molecule-1 (VCAM-1) expression were analyzed at protein and message levels.
Main Results:
- n-LDL significantly increased the adherence of phorbol myristate acetate (PMA)-stimulated U937 cells, monocytes, and neutrophils to ECs.
- Anti-ICAM-1 antibodies blocked the increased adherence, indicating ICAM-1's critical role.
- n-LDL treatment led to a twofold increase in ICAM-1 protein and message levels.
- Increased message levels for E-selectin and VCAM-1 were observed, but without significant protein level changes.
Conclusions:
- n-LDL enhances endothelial cell adherence primarily through the upregulation of ICAM-1.
- This increased adherence is a proinflammatory response to n-LDL exposure.
- n-LDL-induced changes in EC function represent an early stage in the development of atherosclerosis.