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PAR-2 activation, PGE₂, and COX-2 in human asthmatic and nonasthmatic airway smooth muscle cells

Department of Pharmacology, University of Sydney, New South Wales 2006, Australia

Submitted 5 December 2002 ; accepted in final form 13 May 2003

The protease-activated receptor-2 (PAR-2) is present on human airway smooth muscle (ASM) cells and can be activated by mast cell tryptase, trypsin, or an activating peptide (AP). Trypsin induced significant increases in PGE₂ release from human ASM cells after 6 and 24 h and also induced cyclooxygenase (COX)-2 mRNA expression and COX-2 protein. Tryptase and the PAR-2 AP did not alter PGE₂ release or COX-2 protein levels, suggesting a lack of PAR-2 involvement. When we compared results in asthmatic and nonasthmatic muscle cells, both trypsin and bradykinin induced less PGE₂ from asthmatic ASM cells, and bradykinin induced significantly less COX-2 mRNA in asthmatic cells. Significantly less PGE₂ was released from proliferating ASM cells from asthmatic patients. In conclusion, trypsin induces PGE₂ release and COX-2 in human ASM cells, which is unlikely to be via PAR-2 activation. In addition, ASM cells from asthmatic patients produce significantly less PGE₂ and COX-2 compared with nonasthmatic cells. These findings may contribute to the increase in muscle mass evident in asthmatic airways.

protease-activated receptor; tryptase; asthma; prostaglandin E₂; cyclooxygenase-2

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