Effects of prostagladin E2 on gel-forming mucin secretion in normal human nasal epithelial cells

Conclusion. The findings of this study indicate that prostaglandin E-2 (PGE(2)) induces MUC5AC gene expression and mucin secretion via the EP4 receptor in cultured normal human nasal epithelial cells. Objectives. Recently, PGE2 was found to induce MUC5AC production via an agonist of EP2/EP4, but not EP1/EP3, in normal human airway epithelium. However, the receptor that mediates MUC5AC has not been determined. This study aimed to investigate the MUC5AC mucin gene and mucin secretion by PGE2 and its receptors in cultured normal human nasal epithelial cells. Methods. After treatment with PGE(2) and/or PGE(2) antagonist, gel-forming mucin mRNA expression was determined by reverse transcription-polymerase chain reaction. Total mucin and MUC5AC mucin levels were measured using an immuno-dot blotting assay. Results. PGE2 increased only MUC5AC gene expression and MUC5AC mucin, but not expression of other gel-forming mucin genes. An EP2 receptor antagonist (AH 6809) did not suppress the PGE(2)-induced MUC5AC gene expression or MUC5AC mucin. However, an EP4 receptor antagonist (AH23848) significantly suppressed the level of PGE(2)-induced MUC5AC gene expression and MUC5AC mucin.