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J Appl Physiol 91: 1372-1379, 2001;
8750-7587/01 $5.00
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Vol. 91, Issue 3, 1372-1379, September 2001

Tryptase and agonists of PAR-2 induce the proliferation of human airway smooth muscle cells

Patrick Berger1,2, Diahn-Warng Perng1, Hiran Thabrew1, Steven J. Compton1, Jennifer A Cairns1, Alan R. McEuen1, Roger Marthan2, José-Manuel Tunon De Lara2, and Andrew F. Walls1

1 Immunopharmacology Group, Southampton General Hospital, Southampton SO16 6YD, United Kingdom; and 2 Laboratoire de Physiologie Cellulaire Respiratoire, INSERM E9937, Université Victor Ségalen Bordeaux2, 33076 Bordeaux Cedex, France

Airway remodeling with smooth muscle cell (SMC) hyperplasia is a feature of chronic asthma. We investigated the potential for tryptase, the major secretory product of human mast cells, to act as a growth factor for human airway SMCs. Because this serine protease can activate proteinase-activated receptor-2 (PAR-2), we also examined the actions of SLIGKV, a peptide agonist of PAR-2. Incubation with lung tryptase provoked a twofold increase in [3H]thymidine incorporation; a similar increase in cell numbers was found when we used the MTS assay. The effect was catalytic site dependent, being abolished by the protease inhibitors leupeptin and benzamidine and by heat inactivation of the enzyme. Tryptase-induced DNA synthesis was inhibited by preincubation of the cells with pertussis toxin, calphostin C, or genistein. Transduction mechanisms are thus likely to involve a pertussis toxin-sensitive G protein, protein kinase C, and tyrosine kinase. SLIGKV elicited a response on SMCs similar to that of tryptase. Tryptase could provide an important stimulus for SMC proliferation in asthmatic airways, by acting on PAR-2.

proteinase-activated receptor-2; mast cell


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