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Prostaglandin E2 induces MUC8 gene expression via a mechanism involving ERK MAPK/RSK1/cAMP response element binding protein activation in human airway epithelial cells
- Prostaglandin E2 induces MUC8 gene expression via a mechanism involving ERK MAPK/RSK1/cAMP response element binding protein activation in human airway epithelial cells
- Cho K.-N.; Choi J.Y.; Kim C.-H.; Baek S.J.; Chung K.C.; Moon U.Y.; Lee W.-J.; Koo J.S.; Yoon J.-H.; Kim K.-S.
- Ewha Authors
- Issue Date
- Journal Title
- Journal of Biological Chemistry
- Journal of Biological Chemistry vol. 280, no. 8, pp. 6676 - 6681
- SCI; SCIE; SCOPUS
- Document Type
- MUC8 gene expression is overexpressed in nasal polyp epithelium and is also increased by treatment with inflammatory mediators in nasal epithelial cells. These data suggest that MUC8 may be one of important mucin genes expressed in human airway. However, the mechanisms of various inflammatory mediator-induced MUC8 gene expression in normal nasal epithelial cells remain unclear. We examined the mechanism by which prostaglandin E2 (PGE2), an arachidonic acid metabolite, increases MUC8 gene expression levels. Here, we show that ERK mitogen-activated protein kinase is essential for PGE2-induced MUC8 gene expression in normal human nasal epithelial cells and that p90 ribosomal S 6 protein kinase 1 (RSK1) mediates the PGE2-induced phosphorylation of cAMP-response element binding protein. Our results also indicate that cAMP-response element at the -803 region of the MUC8 promoter is an important site of PGE2-induced MUC8 gene expression. In conclusion, this study gives insights into the molecular mechanism of PGE2-induced MUC8 gene expression in human airway epithelial cells. © 2005 by The American Society for Biochemistry and Molecular Biology, Inc.
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