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1 Department of Pharmacology, University of Sydney, Sydney, NSW, Australia
* To whom correspondence should be addressed. E-mail: judblack{at}med.usyd.edu.au.
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 hours and also induced 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 non-asthmatic 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 non-asthmatic cells. These findings may contribute to the increase in muscle mass evident in asthmatic airways.
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