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Título

Sustained nitric oxide delivery delays nitric oxide-dependent apoptosis in macrophages: Contribution to the physiological function of activated macrophages

AutorHortelano, Sonsoles; Través, Paqui G.; Zeini, Miriam; Álvarez, Alberto; Boscá, Lisardo
Fecha de publicación1-dic-2003
EditorAmerican Association of Immunologists
CitaciónJournal of Immunology 171(11): 6059-6064 (2003)
ResumenTreatment of the macrophage cell line RAW 264.7 with the short-lived NO donor -nitrosoglutathione triggers apoptosis through the release of mitochondrial mediators. However, continuous supply of NO by long-lived NO donors protected cells from apoptosis through mechanisms that involved the maintenance or an increase in the levels of the inhibitor of apoptosis proteins (IAPs) cIAP-1, cIAP-2, and xIAP and decreases in the accumulation of p53 and in the levels and targeting of Bax to the mitochondria. As a result of these changes, the activation of caspases 9 and 3 was notably delayed, expanding the time of viability of the macrophages. Moreover, inhibition of NO synthase 2 activity after 8 h of stimulation of RAW 264.7 cells with LPS and IFN-{gamma} accelerated apoptosis via an increase in the processing and activation of caspases. These data suggest that NO exerts an important role in the autoregulation of apoptosis in macrophages.
Descripción7 pages, 5 figures.
Versión del editorhttp://www.jimmunol.org/cgi/content/full/171/11/6059
URIhttp://hdl.handle.net/10261/24495
ISSN0022-1767
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