P. AkarasereenontC. ThiemermannBarts and The London Queen Mary's School of Medicine and DentistryMahidol University2018-07-042018-07-041996-03-07Biochemical and Biophysical Research Communications. Vol.220, No.1 (1996), 181-1850006291X2-s2.0-0029963821https://repository.li.mahidol.ac.th/handle/20.500.14594/17546Cyclo-oxygenase (COX) exists as two isoforms. In endothelial cells, the induction of COX (COX-2) elicited by endotoxin or inflammatory cytokines is mediated by tyrosine kinase. Here we have investigated whether the induction of COX-2 elicited by IL-1β in human pulmonary epithelial cells (A549) is mediated by tyrosine kinase. The activity of COX-2 was assessed by measuring the accumulation of PGE2by radioimmunoassay. The expression of COX-2 protein was detected by immunoblot using specific antibodies to COX-2. Untreated A549 cells contained no COX-2 protein and released low levels of PGE2(< 0.3 ng/ml for 24 h). A549 cells treated with IL-1β (0.01 to 10 ng/ml) contained COX-2 protein and released greater amounts of PGE2. The increased COX-2 protein and activity in response to IL-1β (10 ng/ml) was inhibited by the tyrosine kinase inhibitors tyrphostin (AG126; 0.015 to 15 μM) or erbstatin (0.004 to 4 μM). Thus, the induction of COX-2 by IL-1β in epithelial cells is mediated by tyrosine kinase.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyArticleSCOPUS10.1006/bbrc.1996.0377