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Titolo:
S-nitrosoglutathione inhibits TNF-alpha-induced NF kappa B activation in neutrophils
Autore:
Fortenberry, JD; Owens, ML; Chen, NX; Brown, LAS;
Indirizzi:
Childrens Healthcare Altanta Egleston, Crit Care Div, Atlanta, GA 30322 USA Childrens Healthcare Altanta Egleston Atlanta GA USA 30322 , GA 30322 USA
Titolo Testata:
INFLAMMATION RESEARCH
fascicolo: 2, volume: 50, anno: 2001,
pagine: 89 - 95
SICI:
1023-3830(200102)50:2<89:SITNKB>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; HUMAN ENDOTHELIAL-CELLS; EXOGENOUS NITRIC-OXIDE; ACUTE LUNG INJURY; DNA FRAGMENTATION; POLYMORPHONUCLEAR NEUTROPHILS; PROINFLAMMATORY CYTOKINES; INDUCED APOPTOSIS; INFLAMMATION; MACROPHAGES;
Keywords:
neutrophils; transcription factor; nitric oxide; nuclear factor-kappa B (NF kappa B);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Fortenberry, JD Childrens Healthcare Altanta Egleston, Crit Care Div, 1405Clifton Rd NE, Atlanta, GA 30322 USA Childrens Healthcare Altanta Egleston1405 Clifton Rd NE Atlanta GA USA 30322
Citazione:
J.D. Fortenberry et al., "S-nitrosoglutathione inhibits TNF-alpha-induced NF kappa B activation in neutrophils", INFLAMM RES, 50(2), 2001, pp. 89-95

Abstract

Objective and Design: Cytokine expression is controlled by transcription factors including NF kappaB, which has recently been found to exist in humanneutrophils. We previously showed that exogenous nitric oxide (NO) inducesneutrophil apoptosis and hypothesized that this NO effect could be mediated by inhibition of NF kappaB activation. Materials and methods: Isolated human neutrophils were incubated with or without S-nitrosoglutathione (GSNO 0.1 mM-5 mM; Sigma) for 2 h. Neutrophils were either unstimulated or stimulated with TNF alpha or n-formyl methionylleucine phenylalanine (fMLP). Viability was assessed by vital dye cytotoxicity assay. After nuclear extraction and measurement of protein concentration, NF kappaB binding was determined by electrophoretic mobility shift assay. Effects of GSNO on activation of I kappaB alpha, which inhibits intranuclear translocation of NF kappaB, were measured by Western immunoblot technique. For comparison, experiments were also performed in the presence of theNF kappaB inhibitor PDTC. Results. TNF alpha increased nuclear NF kappaB activity compared to unstimulated neutrophils (p<0.001, n=5). GSNO (500 <mu>M) decreased TNF alpha -induced NF kappaB activity (p<0.05) and inhibited NF<kappa>B activity whethergiven prior to or during TNF alpha exposure. I kappaB alpha: was significantly degraded at 30 and 120 min of TNF alpha exposure compared to control neutrophils (p<0.05). GSNO exposure (500 <mu>M) inhibited I kappaB alpha degradation in the presence of TNF alpha. PDTC enhanced neutrophil cell death and DNA fragmentation, in association with decreased NF kappaB activity, similar to GSNO effects. Conclusion: Neutrophils possess NF kappaB activity that is increased by stimulation with TNF alpha. GSNO inhibits NF kappaB activity in association with inhibiting TNF alpha -induced degradation of I kappaB alpha. GSNO effects are similar to those seen with NF kappaB inhibition by PDTC. Inhibition of NF kappaB could represent a potential anti-inflammatory effect of GSNO.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 07:04:56