Epithelial P2X purinergic receptor channel expression and function
Amanda L. Taylor, … , Eric J. Sorscher, Erik M. Schwiebert
Amanda L. Taylor, … , Eric J. Sorscher, Erik M. Schwiebert
Published October 1, 1999
Citation Information: J Clin Invest. 1999;104(7):875-884. https://doi.org/10.1172/JCI7270.
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Epithelial P2X purinergic receptor channel expression and function

Abstract

P2X purinergic receptor (P2XR) channels bind ATP and mediate Ca2+ influx — 2 signals that stimulate secretory Cl– transport across epithelia. We tested the hypotheses that P2XR channels are expressed by epithelia and that P2XRs transduce extracellular ATP signals into stimulation of Cl– transport across epithelia. Electrophysiological data and mRNA analysis of human and mouse pulmonary epithelia and other epithelial cells indicate that multiple P2XRs are broadly expressed in these tissues and that they are active on both apical and basolateral surfaces. Because P2X-selective agonists bind multiple P2XR subtypes, and because P2X agonists stimulate Cl– transport across nasal mucosa of cystic fibrosis (CF) patients as well as across non-CF nasal mucosa, P2XRs may provide novel targets for extracellular nucleotide therapy of CF.

Authors

Amanda L. Taylor, Lisa M. Schwiebert, Jeffrey J. Smith, Chris King, Julie R. Jones, Eric J. Sorscher, Erik M. Schwiebert

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Figure 1

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Apical (apm) and basolateral (blm) P2X agonists stimulate ISC across mou...
Apical (apm) and basolateral (blm) P2X agonists stimulate ISC across mouse tracheal epithelial monolayers grown in primary culture. (a) Parallel recordings with and without apical amiloride are shown. Measured current values (in μA/cm2) are shown at points along each record. P2YR-selective agonists were also tested in these experiments. No washing of agonists was performed. (b) Data summary of transient (T) and prolonged (S) ISC stimulated by the agonist, BzBz-ATP. n = 4 with and without amiloride. All stimulated current was significant (P < 0.005). Similar effects were obtained in experiments with α,β-meth-ATP.