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Calcium signaling in human airway goblet cells following purinergic activation

¹Department of Cell and Molecular Physiology, ²Michael Hooker Microscopy Facility, and ³Cystic Fibrosis/Pulmonary Research and Treatment Center, University of North Carolina, Chapel Hill, North Carolina

Submitted 7 March 2006 ; accepted in final form 17 August 2006

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⁺ (Ca) has not been reported. In this article, we describe the results of experiments measuring Ca in primary cultures of human bronchial goblet cells after stimulation with the purinergic agonist adenosine 5'-O-(3-thiotriphosphate) (ATPS) and phorbol 12-myristate 13-acetate (PMA). Ca²⁺ signaling in human goblet cells after purinergic stimulation follows the classic paradigm of a Ca 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 superbasal plateau (155.3 ± 0.2 nM) between 10 and 15 min. The rise in Ca appears to result from a mobilization of intracellular stores, because the transient was nearly abolished by inhibition of PLC with the phosphatidylinositol-specific PLC inhibitor U-73122, and it was not affected significantly by removal of extracellular Ca²⁺. Loading goblet cells with BAPTA inhibited the ATPS-induced Ca²⁺ transient by 86.0 ± 13.1%, relative to control. Finally, in contrast to the massive effects of high doses of PMA (300 nM) on mucin secretion from goblet cells, phorbol ester stimulated a small (27.1 ± 7% of the ATPS control peak), brief rise in Ca. This diminutive signal likely denotes a local Ca²⁺ gradient, which may be associated with the mucin granule exocytotic process.

mucus; exocytosis; purinergic signaling; P2Y₂

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