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Korean Journal of Otolaryngology - Head and Neck Surgery ; : 307-312, 2006.
Artigo em Coreano | WPRIM | ID: wpr-647030

RESUMO

BACKGROUND AND OBJECTIVES: Recently, Prostaglandin E2 (PGE2) was found to induce MUC5AC production via an agonist of E-prostanoid (EP2/EP4), but not EP1/EP3, in normal human airway epithelium. However, the receptor that mediates MUC5AC has not been determined. This study was aimed to investigate the MUC5AC mucin gene and mucin secretion by PGE2 and its receptors in cultured normal human nasal epithelial cells. MATERIALS AND METHOD: After treatment with PGE2 and/or PGE2 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 the MUC5AC gene expressions and MUC5AC mucin, but not the expressions of other gel-forming mucin genes. An EP2 receptor antagonist (AH6809) did not suppress the PGE2-induced MUC5AC gene expression or MUC5AC mucin. However, an EP4 receptor antagonist (AH23848) significantly suppressed the level of PGE2-induced MUC5AC gene expression and MUC5AC mucin. CONCLUSION: These findings indicate that PGE2 induces MUC5AC gene expression and mucin secretion via EP4 receptor in cultured normal human nasal epithelial cells.


Assuntos
Humanos , Dinoprostona , Células Epiteliais , Epitélio , Expressão Gênica , Mucinas , Receptores de Prostaglandina , RNA Mensageiro
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