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PAR-2 activation, PGE[sub 2], and COX-2 in human asthmatic and nonasthmatic airway smooth muscle cells.
- Source :
-
American Journal of Physiology: Lung Cellular & Molecular Physiology . Sep2003, Vol. 29 Issue 3, pL619-L627. 9p. 5 Diagrams, 1 Chart, 7 Graphs. - Publication Year :
- 2003
-
Abstract
- 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 PGE[sub 2] 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 PGE[sub 2] 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 PGE[sub 2] from asthmatic ASM cells, and bradykinin induced significantly less COX-2 mRNA in asthmatic cells. Significantly less PGE[sub 2] was released from proliferating ASM cells from asthmatic patients. In conclusion, trypsin induces PGE[sub 2] 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 PGE[sub 2] and COX-2 compared with nonasthmatic cells. These findings may contribute to the increase in muscle mass evident in asthmatic airways. [ABSTRACT FROM AUTHOR]
- Subjects :
- *SMOOTH muscle
*PROSTAGLANDINS
*CYCLOOXYGENASE 2
*ASTHMA
Subjects
Details
- Language :
- English
- ISSN :
- 10400605
- Volume :
- 29
- Issue :
- 3
- Database :
- Academic Search Index
- Journal :
- American Journal of Physiology: Lung Cellular & Molecular Physiology
- Publication Type :
- Academic Journal
- Accession number :
- 10783739