Abstract
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 E(2) (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.
Highlights
Mechanicochemical proteins produced by airway epithelial cells are essential components of airway mucus, which plays an important role in the protection of the airways from bacterial and viral attack
We examined the mechanism by which prostaglandin E2 (PGE2), an arachidonic acid metabolite, increases MUC8 gene expression levels
Our results indicate that cAMP-response element at the ؊803 region of the MUC8 promoter is an important site of PGE2-induced MUC8 gene expression
Summary
MUC8 gene expression is overexpressed in nasal polyp epithelium and is 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. 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. This study gives insights into the molecular mechanism of PGE2-induced MUC8 gene expression in human airway epithelial cells. We found that extracellular signal-regulated kinase mitogen-activated protein kinase (ERK MAPK) is essential for PGE2-induced MUC8 gene expression in normal human nasal epithelial (NHNE) cells. These studies provide insights into the mechanism of PGE2-induced MUC8 gene expression and extend our understanding of mucin gene overexpression during airway mucosal inflammation
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