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Oxidized LDL-mediated monocyte adhesion to endothelial cells does not involve NFkappaB
A Dwivedi1, E E Anggård, M J Carrier
1Department of Experimental Therapeutics, William Harvey Research Institute, St. Bartholomew's and The Royal London School of Medicine and Dentistry School, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, United Kingdom.
Biochemical and Biophysical Research Communications
|May 26, 2001
Summary
Oxidised LDL (oxLDL) significantly increases monocyte adhesion to endothelial cells, independent of ICAM-1, VCAM-1, and NF-kappaB. This suggests novel mechanisms driving atherogenesis.
Area of Science:
- Cardiovascular Biology
- Atherosclerosis Research
- Endothelial Cell Biology
Background:
- Oxidised LDL (oxLDL) is a critical factor in atherosclerosis development.
- Understanding oxLDL's role in monocyte adhesion is key to understanding atherogenesis.
- Endothelial cell interactions with monocytes are central to plaque formation.
Purpose of the Study:
- To investigate the effect of oxLDL on monocyte adhesion to EA.hy 926 endothelial cells.
- To determine the involvement of ICAM-1, VCAM-1, MCP-1, and NF-kappaB in oxLDL-induced monocyte adhesion.
- To elucidate the mechanisms underlying oxLDL-mediated monocyte recruitment.
Main Methods:
- EA.hy 926 endothelial cells were treated with varying concentrations of oxLDL and unmodified LDL (nLDL).
- Monocyte adhesion assays were performed to quantify cell-cell interactions.
- Expression levels of ICAM-1, VCAM-1, and MCP-1 mRNA were analyzed.
- NF-kappaB activation was assessed via IkappaB-alpha degradation and EMSA.
Main Results:
- OxLDL significantly increased monocyte adhesion in a dose-dependent manner, comparable to TNF-alpha.
- Unmodified LDL did not affect monocyte adhesion.
- Both oxLDL and nLDL elevated MCP-1 mRNA levels.
- OxLDL did not alter ICAM-1 or VCAM-1 expression and did not activate NF-kappaB.
Conclusions:
- Monocyte adhesion to EA.hy 926 cells is enhanced by oxLDL through pathways independent of ICAM-1, VCAM-1, and NF-kappaB.
- These findings suggest the involvement of novel adhesive mechanisms in oxLDL-driven atherogenesis.
- Further research is needed to identify these alternative pathways.