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Involvement of Syk kinase in TNF-induced nitric oxide production by airway epithelial cells
Authors:Ulanova Marina  Marcet-Palacios Marcelo  Muñoz Samira  Asfaha Samuel  Kim Moo-Kyung  Schreiber Alan D  Befus A Dean
Institution:Department of Medicine, University of Alberta, Edmonton, Alta., Canada. marina.ulanova@normed.ca
Abstract:We have recently found that Syk is widely expressed in lung epithelial cells (EC) and participates in beta1 integrin signaling. In this study, we assessed the role of Syk in regulation of NO production. Stimulation of human bronchial EC line HS-24 by TNF caused an increased expression of inducible nitric oxide synthase (iNOS). Inhibition of Syk using siRNA or piceatannol down-regulated the iNOS expression and reduced NO production. This effect occurred in EC simultaneously stimulated via beta1 integrins, suggesting that TNF and beta1 integrins provide co-stimulatory signals. Inhibition of Syk down-regulated TNF-induced p38 and p44/42 MAPK phosphorylation and nuclear translocation of p65 NF-kappaB. Thus, TNF-induced activation of pro-inflammatory signaling in EC leading to enhanced expression of iNOS and NO production was dependent on Syk. Syk-mediated signaling regulates NO production at least partly via activating the MAPK cascade. Understanding the role of Syk in airway EC may help in developing new therapeutic tools for inflammatory lung disorders.
Keywords:Nitric oxide  Lung  Epithelial cells  Intracellular signaling  Syk  Inflammatory responses  TNF
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