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The FASEB Journal Express Article doi:10.1096/fj.05-4585fje
Published online March 29, 2006

Transcriptional regulation of CD38 expression by tumor necrosis factor-{alpha} in human airway smooth muscle cells: role of NF-{kappa}B and sensitivity to glucocorticoids

Bit-Na Kang, K. G. Tirumurugaan, Deepak A. Deshpande, Yassine Amrani, Reynold A. Panettieri, Timothy F. Walseth, and Mathur S. Kannan

E-mail contact: >kanna001@umn.edu

The transmembrane glycoprotein CD38 catalyzes the synthesis of the calcium mobilizing molecule cyclic ADP-ribose from NAD. In human airway smooth muscle (HASM) cells, the expression and function of CD38 are augmented by the inflammatory cytokine tumor necrosis factor-alpha (TNF-{alpha}), leading to increased intracellular calcium response to agonists. A glucocorticoid response element in the CD38 gene has been computationally described, providing evidence for transcriptional regulation of its expression. In the present study, we investigated the effects of dexamethasone, a glucocorticoid, on CD38 expression and ADP-ribosyl cyclase activity in HASM cells stimulated with TNF-{alpha}. In HASM cells, TNF-{alpha} augmented CD38 expression and ADP-ribosyl cyclase activity, which were attenuated by dexamethasone. TNF-{alpha} increased NF-{kappa}B expression and its activation, and dexamethasone partially reversed these effects. TNF-{alpha} increased the expression of I{kappa}B{alpha}, and dexamethasone increased it further. An inhibitor of NF-{kappa}B activation or transfection of cells with I{kappa}B mutants decreased TNF-{alpha}-induced CD38 expression. The results indicate that TNF-{alpha}-induced CD38 expression involves NF-{kappa}B expression and its activation and dexamethasone inhibits CD38 expression through NF-{kappa}B-dependent and -independent mechanisms.-- Kang, B.-N., Tirumurugaan, K. G., Deshpande, D. A., Amrani, Y., Panettieri, R. A., Walseth, T. F., Kannan, M. S. Transcriptional regulation of CD38 expression by tumor necrosis factor-{alpha} in human airway smooth muscle cells: role of NF-{kappa}B and sensitivity to glucocorticoids.




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