The Receptor RAGE as a Progression Factor Amplifying Arachidonate-Dependent Inflammatory and Proteolytic Response in Human Atherosclerotic Plaques
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- 2 September 2003
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation
- Vol. 108 (9) , 1070-1077
- https://doi.org/10.1161/01.cir.0000086014.80477.0d
Abstract
Background— RAGE (receptor for advanced glycation end products [AGEs]) plays a role in diabetic atherosclerosis. Recently, we have demonstrated enhanced expression of cyclooxygenase-2 and PGE synthase-1 (COX-2/mPGES-1) in human symptomatic plaques, and provided evidence that it is associated with metalloproteinase (MMP)-induced plaque rupture. However, the specific transmembrane signaling pathway(s) influencing plaque COX-2/mPGES-1 expression is unknown. The aim of this study was to characterize RAGE expression in human plaques and to correlate it with the inflammatory infiltration, COX-2/mPGES-1 and MMP expression, and with clinical evidence of diabetes. Methods and Results— Plaques obtained from 60 patients undergoing carotid endarterectomy were divided into diabetic and nondiabetic according to clinical evidence of type 2 diabetes. Plaques were subjected to analysis of RAGE, NF-κB, COX-2/mPGES-1, MMP-2 and MMP-9, lipid and oxidized LDL (oxLDL) content, and collagen content by immunohistochemistry and W...Keywords
This publication has 13 references indexed in Scilit:
- Suppression of the Functionally Coupled Cyclooxygenase-2/Prostaglandin E Synthase as a Basis of Simvastatin-Dependent Plaque Stabilization in HumansCirculation, 2003
- RAGE Blockade Stabilizes Established Atherosclerosis in Diabetic Apolipoprotein E–Null MiceCirculation, 2002
- NFκB-dependent Transcriptional Activation during Heat Shock RecoveryJournal of Biological Chemistry, 2001
- N ε-(Carboxymethyl)Lysine Adducts of Proteins Are Ligands for Receptor for Advanced Glycation End Products That Activate Cell Signaling Pathways and Modulate Gene ExpressionJournal of Biological Chemistry, 1999
- Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33)The Lancet, 1998
- Suppression of accelerated diabetic atherosclerosis by the soluble receptor for advanced glycation endproductsNature Medicine, 1998
- Concordant Induction of Prostaglandin E2Synthase with Cyclooxygenase-2 Leads to Preferred Production of Prostaglandin E2over Thromboxane and Prostaglandin D2in Lipopolysaccharide-Stimulated Rat Peritoneal MacrophagesBiochemical and Biophysical Research Communications, 1997
- Oxidized low density lipoprotein inhibits lipopolysaccharide-induced binding of nuclear factor-kappaB to DNA and the subsequent expression of tumor necrosis factor-alpha and interleukin-1beta in macrophages.Journal of Clinical Investigation, 1996
- Activated transcription factor nuclear factor-kappa B is present in the atherosclerotic lesion.Journal of Clinical Investigation, 1996
- Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques.Journal of Clinical Investigation, 1994