title: Er:YAG laser irradiation increases prostaglandin E production via the induction of cyclooxygenase-2 mRNA in human gingival fibroblasts.
abstract: OBJECTIVE
  It has been reported that both prostaglandin E2 (PGE2) and Er:YAG laser irradiation accelerate wound healing. The stimulatory action of laser seems to occur during the proliferative stage of healing by stimulation of prostaglandin E2 and cyclooxygenase-2 (COX-2), which are crucial early mediators in the natural healing process. We have then investigated the effect of Er:YAG laser irradiation on PGE2 production and COX-2 gene expression in human gingival fibroblast in vitro.
  
  
  METHODS
  Cultured fibroblasts were exposed to low-power Er:YAG laser irradiation with an energy density of 3.37 J/cm2. The amount of PGE2 production was measured by enzyme-linked immunosorbent assay (ELISA). COX-2 mRNA level, which is a critical enzyme for PGE2 production, was analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR).
  
  
  RESULTS
  Er:YAG laser significantly increased PGE2 production by human gingival fibroblasts. COX-2 mRNA, which was hardly detectable in control, increased dramatically after irradiation. COX-2 inhibitor, NS398, completely inhibited the PGE2 synthesis stimulated by Er:YAG laser irradiation.
  
  
  CONCLUSIONS
  Our results showed that Er:YAG laser irradiation appears to exert its stimulative action on gingival fibroblasts proliferation through the production of PGE2 via the expression of COX-2. This should be considered as one of the important regulatory pathways to accelerate wound healing after Er:YAG laser irradiation.
authors.affiliation: Periodontology, Department of Hard Tissue Engineering, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan. amir.peri@tmd.ac.jp
authors.forename: A
authors.initials: A
authors.lastname: Pourzarandian
authors.forename: H
authors.initials: H
authors.lastname: Watanabe
authors.forename: S M P M
authors.initials: SM
authors.lastname: Ruwanpura
authors.forename: A
authors.initials: A
authors.lastname: Aoki
authors.forename: K
authors.initials: K
authors.lastname: Noguchi
authors.forename: I
authors.initials: I
authors.lastname: Ishikawa
mesh_terms: D049109:Cell Proliferation; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D015232:Dinoprostone / Q000096:biosynthesis*; D004790:Enzyme Induction / Q000528:radiation effects; D005347:Fibroblasts / Q000166:cytology / Q000201:enzymology / Q000528:radiation effects*; D005881:Gingiva / Q000166:cytology*; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D053685:Laser Therapy; D008565:Membrane Proteins; D009578:Nitrobenzenes / Q000494:pharmacology; D011451:Prostaglandin-Endoperoxide Synthases / Q000096:biosynthesis*; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D013449:Sulfonamides / Q000494:pharmacology; D014945:Wound Healing / Q000528:radiation effects
chemical_list: D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D008565:Membrane Proteins; D009578:Nitrobenzenes; D012333:RNA, Messenger; D013449:Sulfonamides; C080955:N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone; D007213:Indomethacin