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Titolo:
Nitric oxide attenuates H2O2-induced endothelial barrier dysfunction: mechanisms of protection
Autore:
Gupta, MP; Ober, MD; Patterson, C; Al-Hassani, M; Natarajan, V; Hart, CM;
Indirizzi:
Indiana Univ, Med Ctr, Dept Med, Indianapolis, IN 46202 USA Indiana Univ Indianapolis IN USA 46202 pt Med, Indianapolis, IN 46202 USA Richard L Roudebush Vet Affairs Med Ctr, Indianapolis, IN 46202 USA Richard L Roudebush Vet Affairs Med Ctr Indianapolis IN USA 46202 202 USA Johns Hopkins Univ, Dept Med, Baltimore, MD 21224 USA Johns Hopkins Univ Baltimore MD USA 21224 pt Med, Baltimore, MD 21224 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 1, volume: 280, anno: 2001,
pagine: L116 - L126
SICI:
1040-0605(200101)280:1<L116:NOAHEB>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE LUNG INJURY; DEPENDENT PROTEIN-KINASE; CYCLIC-GMP; HYDROGEN-PEROXIDE; LIPID-PEROXIDATION; PULMONARY-ARTERY; SIGNAL-TRANSDUCTION; GUANYLATE CYCLASE; INDUCED INCREASES; PERMEABILITY;
Keywords:
vascular endothelium; hydrogen peroxide; adenosine 3 ',5 '-cyclic monophosphate; guanosine 3 ',5 '-cyclic monophosphate; nitric oxide synthase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
68
Recensione:
Indirizzi per estratti:
Indirizzo: Hart, CM Vet Adm Med Ctr, Pulm & Crit Care Med Sect, 1670 Clairmont Rd, Decatur, GA30033 USA Vet Adm Med Ctr 1670 Clairmont Rd Decatur GA USA 30033 A30033 USA
Citazione:
M.P. Gupta et al., "Nitric oxide attenuates H2O2-induced endothelial barrier dysfunction: mechanisms of protection", AM J P-LUNG, 280(1), 2001, pp. L116-L126

Abstract

Nitric oxide (. NO) attenuates hydrogen peroxide (H2O2)-mediated injury inporcine pulmonary artery endothelial cells (PAECs) and modulates intracellular levels of cGMP and cAMP. We hypothesized that . NO attenuates H2O2-induced PAEC monolayer barrier dysfunction through cyclic nucleotide-dependentsignaling mechanisms. To examine this hypothesis, cultured PAEC monolayerswere treated with H2O2, and barrier function was measured as transmonolayer albumin clearance. H2O2 caused significant PAEC barrier dysfunction that was attenuated by intracellular as well as extracellular . NO generation. . NO increased PAEC cGMP and cAMP levels, but treatment with inhibitors of soluble guanylate cyclase or protein kinase G did not abrogate . NO-mediatedbarrier protection. In contrast, H2O2 decreased protein kinase A activity,and inhibiting protein kinase A abrogated the protective effect of . NO. H2O2-induced barrier dysfunction was not associated with decreased levels ofcGMP or cAMP. 3-Isobutyl-1-methylxanthine and the cGMP analog 8-bromo-cGMPhad little effect on H2O2-mediated endothelial barrier dysfunction, whereas 8-bromo-cAMP plus 3-isobutyl-1-methylxanthine was protective. These results indicate that . NO modulates vascular endothelial barrier function through cAMP-dependent signaling mechanisms.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 21:52:27