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1 Department of Cell & Molecular Physiology, University of North Carolina, Chapel Hill, North Carolina, United States
2 Michael Hooker Microscopy Facility, University of North Carolina, Chapel Hill, North Carolina, United States
3 Department of Cell & Molecular Physiology, University of North Carolina, Chapel Hill, North Carolina, United States; Michael Hooker Microscopy Facility, University of North Carolina, Chapel Hill, North Carolina, United States
* To whom correspondence should be addressed. E-mail: cwdavis{at}med.unc.edu.
Despite the general importance of Ca2+ signaling in signal transduction, and of goblet cell mucin hypersecretion in inflammatory pulmonary diseases, measurement of airway goblet cell intracellular Ca2+ (Ca2+i) has not been reported. In this paper, we describe the results of experiments measuring intracellular Ca2+ in primary cultures of human bronchial goblet cells following stimulation with the purinergic agonist, ATP
S, and PMA. Ca2+ signaling in human goblet cells following purinergic stimulation follows the classical paradigm of a Ca2+i transient from a basal activity of 110 nM to a peak response of 260.1 ± 41.2 nM within 2 min, followed by a long super-basal plateau (155.3 ± 0.2 nM) between 10 - 15 min. The rise in Ca2+i appears to result from a mobilization of intracellular stores, as the transient was nearly abolished by inhibition of PLC with the phosphotidylinositol-specific PLC inhibitor, U73122, and it was not affected significantly by removal of extracellular Ca2+. Loading goblet cells with BAPTA inhibited the ATPgammaS-induced Ca2+ transient by 86.0 ± 13.1%, relative to control. Lastly, in contrast to the massive effects of high doses of PMA (300 nM) on mucin secretion from goblet cells, phorbol ester stimulated but a small (27.1 ± 7% of the ATPS control peak), brief rise in Ca2+i . This diminutive signal likely denotes a local Ca2+ gradient, which may be associated with the mucin granule exocytotic process.
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