Ox-LDL increases OX40L in endothelial cells through a LOX-1-dependent mechanism.

Abstract

Oxidative low-density lipoprotein (Ox-LDL) is a key risk factor for the development of atherosclerosis, and it can stimulate the expression of a variety of inflammatory signals. As a new and highly sensitive inflammation index, OX40L may be a key to understanding the mechanisms that regulate interactions between cells within the vessel wall and inflammatory mediators during the development of atherosclerosis. To investigate whether Ox-LDL regulates OX40L expression through an oxidized LDL-1 receptor (LOX-1)-mediated mechanism, we investigated the effect of different concentrations of Ox-LDL (50, 100, 150 µg/mL) on endothelial cell proliferation and apoptosis. Stimulation with Ox-LDL increased OX40L protein 1.44-fold and mRNA 4.0-fold in endothelial cells, and these effects were inhibited by blocking LOX-1. These results indicate that LOX-1 plays an important role in the chronic inflammatory process in blood vessel walls. Inhibiting LOX-1 may reduce blood vessel inflammation and provide a therapeutic option to limit atherosclerosis progression.

• Authors: Q Dong, R Xiang, D Y Zhang, S Qin
• Journal: Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas (Braz J Med Biol Res) Vol. 46 Issue 9 Pg. 765-70 (Sep 2013) ISSN: 1414-431X [Electronic] Brazil
• PMID: 24068192 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Lipoproteins, LDL
• OLR1 protein, human
• OX40 Ligand
• Scavenger Receptors, Class E
• TNFSF4 protein, human
• oxidized low density lipoprotein

Topics

• Apoptosis (drug effects)
• Atherosclerosis (etiology, prevention & control)
• Cell Cycle
• Cell Proliferation (drug effects)
• Cells, Cultured
• Human Umbilical Vein Endothelial Cells (cytology, drug effects, metabolism)
• Humans
• Immunoblotting
• Lipoproteins, LDL (metabolism, pharmacology, physiology)
• OX40 Ligand (genetics, metabolism)
• Real-Time Polymerase Chain Reaction
• Scavenger Receptors, Class E (metabolism)
• Signal Transduction
• Vasculitis (physiopathology, prevention & control)