Protease-activated receptor-2-mediated Ca 2+ signaling in guinea pig tracheal epithelial cells
Life Sciences, ISSN: 0024-3205, Vol: 71, Issue: 5, Page: 547-558
2002
- 14Citations
- 5Captures
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Metrics Details
- Citations14
- Citation Indexes14
- 14
- CrossRef13
- Captures5
- Readers5
Article Description
The protease-activated receptor-2 (PAR-2), a G protein-coupled receptor activated by trypsin, contributes to the pathogenesis of inflammatory disease including asthma. Here, we examined the mechanisms by which stimulation of PAR-2 induces an increase in intracellular Ca 2+ concentration ([Ca 2+ ]i) in guinea pig tracheal epithelial cells. Trypsin (0.01–3 units/ml) dose-dependently induced a transient increase in [Ca 2+ ]i, the increase being blocked by soybean trypsin inhibitor (SBTI 1 μM). An increase in [Ca 2+ ]i was also induced by an agonist peptide for PAR-2 (SLIGRL-NH 2, 0.001–10 μM) but not by thrombin (3 units/ml, an activator for PAR-1, PAR-3 or PAR-4). Repeated or cross stimulation of trypsin or SLIGRL-NH 2 caused marked desensitization of the [Ca 2+ ]i response. These responses of [Ca 2+ ]i to trypsin and SLIGRL-NH 2 were attenuated by a phospholipase C inhibitor, U-73122, and a Ca 2+ -ATPase inhibitor, thapsigargin (100 nM), while removal of Ca 2+ and a L-type Ca 2+ -channel blocker, verapamil, were without significant effects. Further, trypsin was without effect on the rate of fura 2 quenching by Mn 2+ entry as an indicator of Ca 2+ influx. Thus, stimulation of PAR-2 appears to increase [Ca 2+ ]i through the mobilization of Ca 2+ from intracellular stores probably via phospholipase Cβ-linked generation of a second messenger.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0024320502017058; http://dx.doi.org/10.1016/s0024-3205(02)01705-8; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0037150746&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/12052439; https://linkinghub.elsevier.com/retrieve/pii/S0024320502017058; http://linkinghub.elsevier.com/retrieve/pii/S0024320502017058; http://api.elsevier.com/content/article/PII:S0024320502017058?httpAccept=text/xml; http://api.elsevier.com/content/article/PII:S0024320502017058?httpAccept=text/plain; http://dx.doi.org/10.1016/s0024-3205%2802%2901705-8; https://dx.doi.org/10.1016/s0024-3205%2802%2901705-8
Elsevier BV
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