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Negative regulation by phosphatidylinositol 3-Kinase of inducible nitric oxide synthase expression in macrophages

AutorDíaz-Guerra, María José; Castrillo, Antonio ; Martín-Sanz, Paloma ; Boscá, Lisardo
Fecha de publicación15-may-1999
EditorAmerican Association of Immunologists
CitaciónJournal of Immunology 162(10): 6184-6190 (1999)
ResumenTriggering of the macrophage cell line RAW 264.7 with LPS promotes a transient activation of phosphatidylinositol 3-kinase (PI3-kinase). Incubation of activated macrophages with wortmannin and LY294002, two inhibitors of PI3-kinase, increased the amount of inducible nitric oxide synthase (iNOS) and the synthesis of nitric oxide. Treatment with wortmannin promoted a prolonged activation of NF-{kappa}B in LPS-treated cells as well as an increase in the promoter activity of the iNOS gene as deduced from transfection experiments using a 1.7-kb fragment of the 5' flanking region of the iNOS gene. Cotransfection of cells with a catalytically active p110 subunit of PI3-kinase impaired the responsiveness of the iNOS promoter to LPS stimulation, whereas transfection with a kinase-deficient mutant of p110 maintained the up-regulation in response to wortmannin. These results indicate that PI3-kinase plays a negative role in the process of macrophage activation and suggest that this enzyme might participate in the mechanism of action of antiinflammatory cytokines.
Descripción8 pages, 7 figures.
Versión del editorhttp://www.jimmunol.org/cgi/content/full/162/10/6184
URIhttp://hdl.handle.net/10261/24357
ISSN0022-1767
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