Epinephrine stimulation of anion secretion in the Calu-3 serous cell model.
Calu-3 is a well-differentiated human bronchial cell line with the characteristics of the serous cells of airway submucosal glands. The submucosal glands play a major role in mucociliary clearance because they secrete electrolytes that facilitate airway hydration. Given the significance of both long- and short-term β-adrenergic receptor agonists in the treatment of respiratory diseases, it is important to determine the role of these receptors and their ligands in normal physiological function. The present studies were designed to characterize the effect of epinephrine, the naturally occurring β-adrenergic receptor agonist, on electrolyte transport of the airway serous cells. Interestingly, epinephrine stimulated two anion secretory channels, the cystic fibrosis transmembrane conductance regulator and a Ca(2+)-activated Cl(-) channel, with the characteristics of transmembrane protein 16A, thereby potentially altering mucociliary clearance via multiple channels. Consistent with the dual channel activation, epinephrine treatment resulted in increases in both intracellular cAMP and Ca(2+). Furthermore, the present results extend previous reports indicating that the two anion channels are functionally linked.
Department of Biology, Indiana University Purdue University Indianapolis;
Amiraj
A
Banga
Department of Biology, Indiana University Purdue University Indianapolis;
Stephanie
S
Flaig
Department of Biology, Indiana University Purdue University Indianapolis;
Shanta
S
Lewis
Nephrology Division and.
Seth
S
Winfree
Department of Biology, Indiana University Purdue University Indianapolis; Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana bblazer@iupui.edu.
Bonnie L
BL
Blazer-Yost
D058666:Adrenergic beta-2 Receptor Agonists / Q000494:pharmacology; D000584:Amiloride / Q000494:pharmacology; D000075369:Anoctamin-1; D001692:Biological Transport; D061207:Calcium Ionophores / Q000494:pharmacology; D045744:Cell Line, Tumor; D018118:Chloride Channels / Q000378:metabolism; D002712:Chlorides / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000378:metabolism; D004837:Epinephrine / Q000494:pharmacology / Q000502:physiology*; D062686:Epithelial Sodium Channel Blockers / Q000494:pharmacology; D006801:Humans; D015759:Ionomycin / Q000494:pharmacology; D009363:Neoplasm Proteins / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D013634:Tannins / Q000494:pharmacology
C476213:ANO1 protein, human; D058666:Adrenergic beta-2 Receptor Agonists; D000075369:Anoctamin-1; C505032:CFTR protein, human; D061207:Calcium Ionophores; D018118:Chloride Channels; D002712:Chlorides; D062686:Epithelial Sodium Channel Blockers; D009363:Neoplasm Proteins; D013634:Tannins; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D015759:Ionomycin; D000584:Amiloride; D012964:Sodium; D000242:Cyclic AMP; D004837:Epinephrine
airway epithelia; cystic fibrosis transmembrane conductance regulator; mucociliary clearance; transepithelial ion transport; transmembrane protein 16A