title: Involvement of cyclooxygenase-2 in serum-induced prostaglandin production by human oral gingival epithelial cells.
abstract: The purpose of the present study was to investigate the involvement of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) in prostaglandin (PG) production by human oral gingival epithelial (OGE) cells stimulated with proinflammatory cytokines including interleukin(IL)-1alpha, IL-1alpha and tumor necrosis factor alpha (TNFalpha), and serum. Fetal bovine serum (FBS)-stimulated OGE cells produced significant levels of PGE2, whereas IL-1alpha, IL-1beta and TNFalpha could not induce significant PGE2 production. FBS induced PGE2 production in a dose- and time-dependent manner. NS-398, a selective COX-2 inhibitor, inhibited PGE2 production by FBS-stimulated cells as completely as indomethacin, a non-selective COX-1/COX-2 inhibitor. Expression of COX-2 protein in FBS-stimulated cells was increased, compared with that in unstimulated cells, whereas COX-1 protein expression was similar both in unstimulated and in FBS-stimulated cells. COX-2 mRNA was detected in FBS-stimulated cells, but not in unstimulated cells. We suggest that COX-2 is responsible for PG production by human OGE cells stimulated with serum and that OGE cells may be involved in PG production in periodontal lesions. Selective COX-2 inhibitors, which have the advantage of reduced gastric toxicity, may provide a useful approach to treatment of periodontal disease.
authors.affiliation: Department of Periodontology, Faculty of Dentistry, Tokyo Medical & Dental University, Japan. kazuyuki-noguchi.peri@dent.tmd.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Noguchi
authors.forename: M
authors.initials: M
authors.lastname: Shitashige
authors.forename: H
authors.initials: H
authors.lastname: Endo
authors.forename: H
authors.initials: H
authors.lastname: Kondo
authors.forename: Y
authors.initials: Y
authors.lastname: Yotsumoto
authors.forename: Y
authors.initials: Y
authors.lastname: Izumi
authors.forename: H
authors.initials: H
authors.lastname: Nitta
authors.forename: I
authors.initials: I
authors.lastname: Ishikawa
mesh_terms: D000704:Analysis of Variance; D001769:Blood; D015153:Blotting, Western; D002478:Cells, Cultured; D003470:Culture Media; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D015232:Dinoprostone / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D004305:Dose-Response Relationship, Drug; D004847:Epithelial Cells / Q000187:drug effects / Q000201:enzymology; D015870:Gene Expression / Q000187:drug effects; D005881:Gingiva / Q000166:cytology / Q000187:drug effects* / Q000201:enzymology; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D018836:Inflammation Mediators / Q000494:pharmacology; D007375:Interleukin-1 / Q000494:pharmacology; D007527:Isoenzymes / Q000037:antagonists & inhibitors / Q000235:genetics / Q000494:pharmacology*; D008565:Membrane Proteins; D009578:Nitrobenzenes / Q000494:pharmacology; D011451:Prostaglandin-Endoperoxide Synthases / Q000235:genetics / Q000494:pharmacology*; D012333:RNA, Messenger / Q000187:drug effects; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013223:Statistics as Topic; D013449:Sulfonamides / Q000494:pharmacology; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D003470:Culture Media; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D018836:Inflammation Mediators; D007375:Interleukin-1; D007527:Isoenzymes; D008565:Membrane Proteins; D009578:Nitrobenzenes; D012333:RNA, Messenger; D013449:Sulfonamides; D014409:Tumor Necrosis Factor-alpha; C080955:N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; C496511:PTGS1 protein, human; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone; D007213:Indomethacin