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Am J Physiol Cell Physiol 277: C1050-C1057, 1999;
0363-6143/99 $5.00
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Vol. 277, Issue 6, C1050-C1057, December 1999

EDITORIAL FOCUS
Involvement of JAK2 and MAPK on type II nitric oxide synthase expression in skin-derived dendritic cells

M. T. Cruz1,2, C. B. Duarte2, M. Gonçalo3, A. P. Carvalho2, and M. C. Lopes1,2

1 Faculdade de Farmácia e 3 Faculdade de Medicina (Servico de Dermatologia), 2 Centro de Neurociências, Universidade de Coimbra, 3000 Coimbra, Portugal

In this report, we demonstrate that a fetal mouse skin-derived dendritic cell line produces nitric oxide (NO) in response to the endotoxin [lipopolysaccharide (LPS)] and to cytokines [tumor necrosis factor-alpha (TNF-alpha ) and granulocyte-macrophage colony-stimulating factor (GM-CSF)]. Expression of the inducible isoform of NO synthase (iNOS) was confirmed by immunofluorescence with an antibody against iNOS. The tyrosine kinase inhibitor genistein decreased LPS- and GM-CSF-induced nitrite (NO-2) production. The effect of LPS and cytokines on NO-2 production was inhibited by the Janus kinase 2 (JAK2) inhibitor tyrphostin B42. The p38 mitogen-activated protein kinase (p38 MAPK) inhibitor SB-203580 also reduced the NO-2 production evoked by LPS, TNF-alpha , or GM-CSF, but it was not as effective as tyrphostin B42. Inhibition of MAPK kinase with PD-098059 also slightly reduced the effect of TNF-alpha or GM-CSF on NO-2 production. Immunocytochemistry studies revealed that the transcription factor nuclear factor-kappa B was translocated from the cytoplasm into the nuclei of fetal skin-derived dendritic cells (FSDC) stimulated with LPS, and this translocation was inhibited by tyrphostin B42. Our results show that JAK2 plays a major role in the induction of iNOS in FSDC.

mitogen-activated protein kinase; Janus kinase 2; nuclear factor-kappa B


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