Publication: The induction of cyclooxygenase-2 in IL-1β-treated endothelial cells is inhibited by prostaglandin E<inf>2</inf>through cAMP
Issued Date
1999-12-01
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09629351
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2-s2.0-0033494228
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Mahidol University
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SCOPUS
Bibliographic Citation
Mediators of Inflammation. Vol.8, No.6 (1999), 287-294
Suggested Citation
Pravit Akarasereenont, Kitirat Techatrisak, Sirikul Chotewuttakorn, Athiwat Thaworn The induction of cyclooxygenase-2 in IL-1β-treated endothelial cells is inhibited by prostaglandin E<inf>2</inf>through cAMP. Mediators of Inflammation. Vol.8, No.6 (1999), 287-294. Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/25323
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Title
The induction of cyclooxygenase-2 in IL-1β-treated endothelial cells is inhibited by prostaglandin E<inf>2</inf>through cAMP
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Abstract
Prostaglandins (PGs) have numerous cardiovascular and inflammatory effects. Cyclooxygenase (COX), which exists as COX-1 and COX-2 isoforms, is the first enzyme in the pathway in which arachidonic acid is converted to PGs. Prostaglandin E2(PGE2) exerts a variety of biological activities for the maintenance of local homeostasis in the body. Elucidation of PGE2involvement in the signalling molecules such as COX could lead to potential therapeutic interventions. Here, we have investigated the effects of PGE2on the induction of COX-2 in human umbilical vein endothelial cells (HUVEC) treated with interleukin-1β (IL-1β 1 ng/ml). COX activity was measured by the production of 6-keto-PGF(1α), PGE2, PGF(2α) and thromboxane B2(TXB2) in the presence of exogenous arachidonic acids (10 μM for 10 min) using enzyme immunoassay (EIA). COX-1 and COX-2 protein was measured by immunoblotting using specific antibody. Untreated HUVEC contained only COX-1 protein while IL-1β treated HUVEC contained COX-1 and COX-2 protein. PGE2(3 μM for 24h) did not affect on COX activity and protein in untreated HUVEC. Interestingly, PGE2(3 μM for 24h) can inhibit COX-2 protein, but not COX-1 protein, expressed in HUVEC treated with IL-1β. This inhibition was reversed by coincubation with forskolin (100 μM). The increased COX activity in HUVEC treated with IL-1β was also inhibited by PGE2(0.03, 0.3 and 3 μM for 24h) in a dose-dependent manner. Similarly, forskolin (10, 50 or 100 μM) can also reverse the inhibition of PGE2 on increased COX activity in IL-1β treated HUVEC. The results suggested that (i) PGE2can initiate negative feedback regulation in the induction of COX-2 elicited by IL-1β in endothelial cells, (ii) the inhibition of PGE2on COX-2 protein and activity in IL-1β treated HUVEC is mediated by cAMP and (iii) the therapeutic use of PGE2in the condition which COX-2 has been involved may have different roles.