Induction of nitric oxid esynthase(NOS) by soluble glucocorticoid induced tumor necrosis factor receptor(sGITR) is modulated by IFN-g in murine macrophage
Experimental & Molecular Medicine
; : 175-180, 2003.
Article
em En
| WPRIM
| ID: wpr-10314
Biblioteca responsável:
WPRO
ABSTRACT
Earlier study showed that glucocorticoid induced tumor necrosis factor receptor (GITR), a new TNFR family, activated murine macrophages to express inducible nitric oxide synthase (iNOS) and to generate nitric oxide (NO). A possible involvement of pro-inflammatory cytokines on NO production by GITR was investigated in vitro systems and signaling molecules contributing to sGITR-induced iNOS production are determined in Raw 264.7 cells, a murine macrophage cell line. The result showed that the synergy was afforded by the combination of GITR with IFN-gamma in a dose-dependent manner but IFN-gamma alone was not able to induce NOS. No effects were observed with TNF-alpha, IL-1beta, or IL-6 co-treated with GITR. To determine signaling molecules contributing to sGITR-induced iNOS production, a specific inhibitor for signal pathway proteins tested showed that PDTC (NF- kB) and genistein (tyrosine kinase) inhibited NOS induction significantly, while sodium orthovanadate (tyrosine phosphatase) potentiated NOS expression. These results suggest that activations of NF-kB were involved in induction of iNOS by GITR and IFN-gamma priming caused earlier and stronger NF-kB activation.
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Índice:
WPRIM
Assunto principal:
Proteínas Tirosina Quinases
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Células Cultivadas
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Indução Enzimática
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Citocinas
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NF-kappa B
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Interferon gama
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Proteínas Tirosina Fosfatases
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Receptores de Fator de Crescimento Neural
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Receptores do Fator de Necrose Tumoral
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Óxido Nítrico Sintase
Limite:
Animals
Idioma:
En
Revista:
Experimental & Molecular Medicine
Ano de publicação:
2003
Tipo de documento:
Article