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Titolo:
Inhibition of oxidant-induced barrier disruption and protein tyrosine phosphorylation in Caco-2 cell monolayers by epidermal growth factor
Autore:
Rao, R; Baker, RD; Baker, SS;
Indirizzi:
MedSAniv S Carolina, Dept Pediat, Div Gastroenterol, Charleston, SC 29403 U Med Univ S Carolina Charleston SC USA 29403 terol, Charleston, SC 29403 U
Titolo Testata:
BIOCHEMICAL PHARMACOLOGY
fascicolo: 6, volume: 57, anno: 1999,
pagine: 685 - 695
SICI:
0006-2952(19990315)57:6<685:IOOBDA>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
SUCRASE-ISOMALTASE EXPRESSION; REACTIVE OXYGEN METABOLITES; RAT GASTRIC-MUCOSA; PARACELLULAR PERMEABILITY; ONTOGENIC RESPONSE; HYDROGEN-PEROXIDE; FACTOR RECEPTOR; FREE-RADICALS; STRESS; MODEL;
Keywords:
epithelium; intestine; permeability; tyrosine kinase; tight junction; EGF;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Rao, R Medleston, Carolina, Dept Pediat, Div Gastroenterol, 158 Rutledge Ave, Char Med Univ S Carolina 158 Rutledge Ave Charleston SC USA 29403 , Char
Citazione:
R. Rao et al., "Inhibition of oxidant-induced barrier disruption and protein tyrosine phosphorylation in Caco-2 cell monolayers by epidermal growth factor", BIOCH PHARM, 57(6), 1999, pp. 685-695

Abstract

The effect of epidermal growth factor (EGF) on the H2O2-induced increase in paracellular permeability in Caco-2 and T-84 cell monolayers was evaluated to examine the role of EGF in intestinal mucosal protection from oxidative stress. Oxidative stress was induced by exposing cell monolayers to H2O2 or a mixture of xanthine oxidase + xanthine (XO + X). Paracellular permeability was assessed by measuring transepithelial electrical resistance (TER),sodium chloride dilution potential, and unidirectional flux of [H-3]mannitol. H2O2 (0.1 to 5.0 mM) reduced TER and dilution potential and increased mannitol flux. Administration of EGF delayed H2O2 and XO f X-induced changesin TER, dilution potential, and [H-3]mannitol flux. This protective effectof apically or basally administered EGF was concentration-related, with A(50) (95% confidence limits) values of 2.1 (1.17 to 4.34) and 6.0 (4.31 to 8.34) nM, respectively. The EGF-mediated protection was prevented by treatment of cell monolayers with genistein (10 mu M), a tyrosine kinase inhibitor. H2O2 and XO + X also induced tyrosine phosphorylation of a number of proteins in Caco-2 and T-84 cell monolayers. EGF treatment inhibited the oxidant-induced tyrosine phosphorylation of proteins, particularly those with a molecular mass of 110-220 kDa. Treatment of Caco-2 cells with anti-transforming growth factor-or antibodies potentiated the H2O2-induced changes in TER, dilution potential, and mannitol flux. These studies demonstrated that anEGF receptor-mediated mechanism delays oxidant-induced disruption of the epithelial barrier function, possibly by suppressing the oxidant-induced tyrosine phosphorylation of proteins. (C) 1999 Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 16/07/20 alle ore 19:43:16