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• W1964590512 endingPage "212" @default.
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• W1964590512 abstract "The role of activator protein-1 (AP-1) in tumor necrosis factor-alpha (TNF-alpha)-induced interleukin-8 (IL-8) gene expression was evaluated. We showed that TNF-alpha activates AP-1 in the transformed endothelial cell line ECV304 by transient transfections of IL-8 promoter construct pGL-3BF(2). Mutation of either the AP-1 site or the NF-IL-6 site on the IL-8 promoter suppressed the TNF-alpha-induced activation, suggesting cooperation between these transcription factors and transcription factor NF-kappaB. Overexpression of dominant negative mutants of c-Jun suppressed AP-1-driven transcription of the IL-8 promoter following stimulation by TNF-alpha, suggesting that cooperative interaction between AP-1 and NF-kappaB is essential for IL-8 transcription in the presence of TNF-alpha. We also showed that nitric oxide (NO), in the form of an exogenous NO donor, suppressed the level of activation of the AP-1 subunit, c-Jun, by down-regulation of c-Jun NH2 terminal kinase. This down-regulation could be the putative mechanism of action for NO-mediated inhibition of IL-8 secretion in activated endothelium. These observations suggest for the first time that NO has broad suppressive activities on various proinflammatory effectors in activated endothelium." @default.
• W1964590512 created "2016-06-24" @default.
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• W1964590512 date "2001-06-01" @default.
• W1964590512 modified "2023-09-27" @default.
• W1964590512 title "Nitric Oxide Suppresses IL-8 Transcription by Inhibiting C-Jun N-Terminal Kinase-Induced AP-1 Activation" @default.
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• W1964590512 doi "https://doi.org/10.1006/excr.2001.5218" @default.
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