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Vol. 62, Issue 5, 1112-1118, November 2002
Induces MUC2 and MUC5AC Synthesis through
Cyclooxygenase-2 in NCI-H292 Cells
Departments of Otorhinolaryngology (Y.-D.K., E.-J.K., S.-Y.S.,
S.-K.Y.) and Biochemistry and Molecular Biology (D.-W.P., S.-H.B.),
College of Medicine, Yeungnam University, Daegu, Korea
Interleukin-1
(IL-1) has been implicated in the pathogenesis of
inflammatory diseases of the airway. In this study, we investigated the
regulation of MUC2 and MUC5AC expression and of their regulatory mechanisms through cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2). Cells activated by IL-1 showed
increased COX-2, MUC2, and MUC5AC expressions at both the mRNA and
protein levels. Mucin production was blocked by the selective COX-2
inhibitor NS398, and PGE2 directly induced MUC2 and MUC5AC
expression at both the mRNA and protein levels in a dose-dependent
manner. These results suggest a role for PGE2 in
IL-1-induced mucin synthesis in NCI-H292 cells. To investigate the
roles of molecules upstream of COX-2 in mucin regulation, we examined
the role of mitogen-activated protein kinases (MAPKs). Cells activated
by IL-1 showed increased extracellular signal-regulated kinase
(ERK)1/2 and p38 phosphorylation, and IL-1-induced MUC2 and MUC5AC
production was blocked by the ERK pathway inhibitor PD98059 or the p38
inhibitor SB203580. The inhibition of both MAPKs reduced
IL-1-induced COX-2 expression and PGE2 synthesis.
Furthermore, the addition of PGE2 to cells overcame the
inhibitory effects of both MAPK inhibitors in IL-1-induced mucin
production. These results indicate that in human pulmonary epithelial
cells, IL-1 activates ERK or p38 to induce COX-2 production, which
in turn induces MUC2 and MUC5AC production.
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