ArticleBritish journal of pharmacology2000
Effect of protease-activated receptor (PAR)-1, -2 and -4-activating peptides, thrombin and trypsin in rat isolated airways.
Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 51 citations in OpenAlex.
- Protease-activated receptors in health and disease.Physiological reviews · 2023Review
- RGS4 promotes allergen- and aspirin-associated airway hyperresponsiveness by inhibiting PGE2 biosynthesis.The Journal of allergy and clinical immunology · 2020Article
- Protease-activated receptor 2 activates airway apical membrane chloride permeability and increases ciliary beating.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- A highly potent agonist to protease-activated receptor-2 reveals apical activation of the airway epithelium resulting in Ca2+-regulated ion conductance.American journal of physiology. Cell physiology · 2014Article
- Novel small airway bronchodilator responses to rosiglitazone in mouse lung slices.American journal of respiratory cell and molecular biology · 2014Article
- Biased signalling and proteinase-activated receptors (PARs): targeting inflammatory disease.British journal of pharmacology · 2014Review
- Neutrophil elastase induces MUC5AC secretion via protease-activated receptor 2.Molecular and cellular biochemistry · 2013Article
- Allergic sensitization enhances anion current responsiveness of murine trachea to PAR-2 activation.Pflugers Archiv : European journal of physiology · 2012Article
- Protease-activated receptors and prostaglandins in inflammatory lung disease.British journal of pharmacology · 2009Review
- Proteinases and signalling: pathophysiological and therapeutic implications via PARs and more.British journal of pharmacology · 2008Review
- Proteinase-activated receptors in the lower urinary tract.Naunyn-Schmiedeberg's archives of pharmacology · 2007Review
- Innate immune responses to environmental allergens.Clinical reviews in allergy & immunology · 2006Review
- Stimulation of protease-activated receptor-2 inhibits airway eosinophilia, hyperresponsiveness and bronchoconstriction in a murine model of allergic inflammation.British journal of pharmacology · 2005Article
- Proteinase-activated receptor-4: evaluation of tethered ligand-derived peptides as probes for receptor function and as inflammatory agonists in vivo.British journal of pharmacology · 2004Article
- Evidence for the presence of functional protease activated receptor 4 (PAR4) in the rat colon.Gut · 2004Article
- Effect of Protease-Activated Receptor-2-Activating Peptide on Guinea Pig Airway Resistance and Isolated Tracheal Strips.Journal of microscopy and ultrastructureArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mechanisms of relaxation and contraction to protease-activated receptor- (PAR) tethered ligand peptides (SFLLRN/TFLLR, SLIGRL and GYPGKF (all C-terminally amidated) for PAR1, PAR2 and PAR4, respectively) and enzymes (thrombin and trypsin) were investigated in isolated segments of rat trachea, main and first order intrapulmonary bronchi. In airway segments previously exposed to SLIGRL, SFLLRN caused contractions that were potentiated by indomethacin, but were independent of mast cell degranulation. Contractions to TFLLR in the intrapulmonary bronchi were similarly potentiated by indomethacin. SLIGRL caused epithelium-dependent relaxations which were unaffected by N(G)-nitro-L-arginine, 1-H-oxodiazol-[1,2,4]-[4,3-a]quinoxaline-1-one or zinc-protoporphyrin-IX but were abolished by haemoglobin in all three regions of the airways. Relaxations to SLIGRL were markedly attenuated by indomethacin only in the main and intrapulmonary bronchi. GYPGKF caused epithelium-dependent relaxations in all three regions of the airway which were only significantly inhibited by indomethacin in the intrapulmonary bronchi. In general, thrombin and trypsin failed to cause any response in the airways tested. Intense PAR2-immunoreactivity was observed on airway epithelium. PAR1-immunoreactivity was faint on airway epithelium and smooth muscle, but was prevalent in mast cells. These findings indicate that PAR2 and possibly PAR4 present on rat airway epithelia mediate smooth muscle relaxation via cyclo-oxygenase-dependent and -independent mechanisms. PAR1-mediated contractions were most likely due to activation of smooth muscle receptors. The general failure of thrombin and trypsin to cause responses which may have been due to endogenous protease inhibitors, highlights the need for caution in assessing pathophysiological roles for PARs if only enzymes are used to activate PARs.
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