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Titolo:
Peroxynitrite causes endothelial cell monolayer barrier dysfunction
Autore:
Knepler, JL; Taher, LN; Gupta, MP; Patterson, C; Pavalko, F; Ober, MD; Hart, CM;
Indirizzi:
Richard L Roudebush Vet Affairs Med Ctr, Dept Med, Indianapolis, IN 46202 USA Richard L Roudebush Vet Affairs Med Ctr Indianapolis IN USA 46202 202 USA Richard L Roudebush Vet Affairs Med Ctr, Dept Physiol, Indianapolis, IN 46202 USA Richard L Roudebush Vet Affairs Med Ctr Indianapolis IN USA 46202 202 USA Indiana Univ, Med Ctr, Indianapolis, IN 46202 USA Indiana Univ Indianapolis IN USA 46202 ed Ctr, Indianapolis, IN 46202 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
fascicolo: 3, volume: 281, anno: 2001,
pagine: C1064 - C1075
SICI:
0363-6143(200109)281:3<C1064:PCECMB>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
INHALED NITRIC-OXIDE; ACUTE LUNG INJURY; RESPIRATORY-DISTRESS SYNDROME; HYDROGEN-PEROXIDE; TYROSINE PHOSPHORYLATION; PROTEIN-PHOSPHORYLATION; VASCULAR-PERMEABILITY; SUPEROXIDE-DISMUTASE; NITRATION; ACCUMULATION;
Keywords:
nitrotyrosine; actin; catenin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Hart, CM Atlanta Vet Affairs Med Ctr, Div Pulm & Crit Care Med, 151-P,1670Clairmont Rd, Decatur, GA 30033 USA Atlanta Vet Affairs Med Ctr 151-P,1670Clairmont Rd Decatur GA USA 30033
Citazione:
J.L. Knepler et al., "Peroxynitrite causes endothelial cell monolayer barrier dysfunction", AM J P-CELL, 281(3), 2001, pp. C1064-C1075

Abstract

Nitric oxide (. NO) attenuates hydrogen peroxide (H2O2)-mediated barrier dysfunction in cultured porcine pulmonary artery endothelial cells (PAEC) (Gupta MP, Ober MD,. Patterson C, Al-Hassani M, Natarajan V, and Hart, CM. AmJ Physiol Lung Cell Mol Physiol 280: L116-LI26, 2001). However, . NO rapidly combines with superoxide (O-2(-)) to form the powerful oxidant peroxynitrite (ONOO-), which we hypothesized would cause PAEC monolayer barrier dysfunction. To test this hypothesis, we treated PAEC with ONOO- (500 muM) or 3-morpholinosydnonimine hydrochloride (SIN-1; 1-500 muM). SIN-1-mediated ONOO- formation was confirmed by monitoring the oxidation of dihydrorhodamine 123 to rhodamine. Both ONOO- and SIN-1 increased albumin clearance (P < 0.05) in the absence of cytotoxicity and altered the architecture of the cytoskeletal proteins actin and <beta>-catenin as detected by immunofluorescent confocal imaging. ONOO--induced barrier dysfunction was partially reversible and was attenuated by cysteine. Both ONOO- and SIN-1 nitrated tyrosine residues, including those on beta -catenin and actin, and oxidized proteins in PAEC. The introduction of actin treated with ONOO- into PAEC monolayers via liposomes also resulted in barrier dysfunction. These results indicate that ONOO- directly alters endothelial cytoskeletal proteins, leading to barrier dysfunction.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 14/07/20 alle ore 05:04:45