Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
Volume 1744, Issue 2, Pages 213-223Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbamcr.2005.03.007
Keywords
TNF alpha; ROS; NADPH oxidase; mitochondria; RAGE; HUVEC
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Funding
- NHLBI NIH HHS [HL67281] Funding Source: Medline
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Engagement of the receptor for advanced glycation end products (RAGE) by its signal transduction ligands is implicated in the development and progression of atherosclerosis. TNF alpha, a proinflammatory cytokine, is a potent inducer of RAGE expression in endothelial cells. In the present study, we demonstrate that reactive oxygen species (ROS) generated by TNF alpha stimulated human umbilical vein endothelial cells (HUVECs) induce RAGE expression. The complex III of mitochondrial respiratory chain appears to be the primary source of ROS. The gp91phox subunit of NADPH oxidase appears to be the source of ROS that induces TNF alpha-dependent mitochondrial ROS generation and subsequent RAGE expression. We also demonstrate that the ROS-mediated RAGE induction occurs via activation of NF-kappa B, a proinflammatory transcription factor. Thus, stimulation of HUVECs by TNF alpha evokes the following sequence of events: stimulation of NADPH oxidase --> generation of ROS --> activation of the mitochondrial respiratory chain --> stimulation of NF-kappa B activity --> induction of RAGE expression. (C) 2005 Elsevier B.V.All rights reserved.
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