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Titolo:
Activation of NADPH oxidase by AGE links oxidant stress to altered gene expression via RAGE
Autore:
Wautier, MP; Chappey, O; Corda, S; Stern, DM; Schimidt, AM; Wautier, JL;
Indirizzi:
Hop Lariboisiere, Lab Biol Vasc & Cellulaire, EA 1557, F-75475 Paris 10, France Hop Lariboisiere Paris France 10 aire, EA 1557, F-75475 Paris 10, France Hop Lariboisiere, Lab Biol Vasc & Cellulaire, F-75475 Paris, France Hop Lariboisiere Paris France F-75475 Cellulaire, F-75475 Paris, France INSERM, U76, F-75475 Paris, France INSERM Paris France F-75475INSERM, U76, F-75475 Paris, France Biophys Hop Lariboisiere, Lab Microcirculat, F-75475 Paris, France BiophysHop Lariboisiere Paris France F-75475 lat, F-75475 Paris, France Columbia Univ Coll Phys & Surg, New York, NY 10032 USA Columbia Univ Coll Phys & Surg New York NY USA 10032 w York, NY 10032 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
fascicolo: 5, volume: 280, anno: 2001,
pagine: E685 - E694
SICI:
0193-1849(200105)280:5<E685:AONOBA>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLYCATION END-PRODUCTS; CULTURED ENDOTHELIAL-CELLS; COLONY-STIMULATING FACTOR; CALCIUM-BINDING PROTEINS; MAILLARD REACTION; DIABETIC VASCULOPATHY; SUPEROXIDE PRODUCTION; RADICAL GENERATION; SIGNALING PATHWAYS; NEURITE OUTGROWTH;
Keywords:
diabetes; renal failure; glycation; receptors; cellular activation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
60
Recensione:
Indirizzi per estratti:
Indirizzo: Wautier, JL Hop Lariboisiere, Lab Biol Vasc & Cellulaire, EA 1557, F-75475Paris 10, France Hop Lariboisiere Paris France 10 7, F-75475 Paris 10, France
Citazione:
M.P. Wautier et al., "Activation of NADPH oxidase by AGE links oxidant stress to altered gene expression via RAGE", AM J P-ENDO, 280(5), 2001, pp. E685-E694

Abstract

Engagement of the receptor for advanced glycation end products (RAGE) by products of nonenzymatic glycation/oxidation triggers the generation of reactive oxygen species (ROS), thereby altering gene expression. Because dissection of the precise events by which ROS are generated via RAGE is relevant to the pathogenesis of complications in AGE-related disorders, such as diabetes and renal failure, we tested the hypothesis that activation of NADPH oxidase contributed, at least in part, to enhancing oxidant stress via RAGE. Here we show that incubation of human endothelial cells with AGEs on the surface of diabetic red blood cells, or specific AGEs, (carboxymethyl)-lysine (CML)-modified adducts, prompted intracellular generation of hydrogen peroxide, cell surface expression of vascular cell adhesion molecule-1, and generation of tissue factor in a manner suppressed by treatment with diphenyliodonium, but not by inhibitors of nitric oxide. Consistent with an important role for NADPH oxidase, although macrophages derived from wild-type miceexpressed enhanced levels of tissue factor upon stimulation with AGE, macrophages derived from mice deficient in a central subunit of NADPH oxidase, gp91phox, failed to display enhanced tissue factor in the presence of AGE. These findings underscore a central role of NADPH oxidase in AGE-RAGE-mediated generation of ROS and provide a mechanism for altered gene expression in AGE-related disorders.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/10/20 alle ore 14:53:57