muramidase and 4-4--dinitro-2-2--stilbenedisulfonic-acid

We evaluated the relationship between apical surface fluid (ASF) and protein secretion in Calu-3 cells grown at an air-liquid interface. Calu-3 monolayers responded to forskolin, a cystic fibrosis transmembrane regulator (CFTR) channel agonist, by secreting a significant amount of ASF. Such a response from Calu-3 monolayers was not observed with CFTR channel blockers glybenclamide and DPC. Other ion channel mediators, PGF-2alpha, PMA, DNDS, and DIDS, had no effect on Calu-3 ASF secretion. Forskolin decreased Calu-3 protein secretion and glybenclamide increased protein secretion. Similarly, forskolin decreased Calu-3 lysozyme secretion, whereas glybenclamide and DPC increased lysozyme secretion. We observed significant changes in Calu-3 fluid and protein secretions with ion channel mediators known to alter CFTR activity. Our results demonstrate a functional link between fluid and protein secretions in Calu-3 apical surface and suggested a possible involvement of CFTR in these processes.

Topics: 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; Anti-Arrhythmia Agents; Body Fluids; Cell Line; Cell Polarity; Colforsin; Cystic Fibrosis Transmembrane Conductance Regulator; Dinoprost; Epithelial Cells; Glyburide; Humans; Muramidase; Oxytocics; Respiratory Mucosa; Stilbenes; Tetradecanoylphorbol Acetate