title: The role of cyclooxygenase-2 in lumbar disc herniation.
abstract: METHODS
  The expression of cyclooxygenase-2 was studied immunohistologically in specimens from lumbar disc herniation. The cultured disc cells also were examined to evaluate the significance of cyclooxygenase-2, which might be involved in the pathogenesis of lumbar disc herniation.
  
  
  OBJECTIVE
  To investigate whether cyclooxygenase-2 might be involved in the pathogenesis of lumbar disc herniation.
  
  
  BACKGROUND
  Prostaglandin E2 is one of the most important mediators contributing to pathogenetic components of lumbar disc herniation. Cyclooxygenase-2, the rate-limiting enzyme of prostaglandin E2 synthesis, has been identified and extensively investigated in other inflammatory diseases. However, the role of cyclooxygenase-2 in lumbar disc herniation has never been addressed.
  
  
  METHODS
  Fifteen specimens from patients with lumbar disc herniation and five control discs from traumatic burst fracture were harvested. The expression of cyclooxygenase-2 was evaluated immunohistologically. The ability of cultured disc cells to produce prostaglandin E2 with inflammatory stimulus in the presence or absence of a selective inhibitor of cyclooxygenase-2 was investigated. At the same time, the induction of cyclooxygenase-2 mRNA of these cells by reverse transcriptase-polymerase chain reaction was detected. The manner in which this prostaglandin E2 production could be suppressed by various doses of a cyclooxygenase-2 inhibitor also was investigated.
  
  
  RESULTS
  Immunohistologically, the expression of cyclooxygenase-2 was observed only in the lumbar disc herniation specimens. The cultured cells had a strong ability to produce prostaglandin E2 coinciding with cyclooxygenase-2 mRNA induction. A selective inhibitor of cyclooxygenase-2 inhibited this prostaglandin E2 production in a dose-dependent manner.
  
  
  CONCLUSIONS
  Cyclooxygenase-2 might be involved in the pathogenesis of lumbar disc herniation through upregulation of prostaglandin E2 production.
authors.affiliation: Department of Orthopaedic Surgery, Kobe University School of Medicine, Kobe, Japan. hm0617@med.kobe-u.ac.jp
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Miyamoto
authors.forename: Ryuichi
authors.initials: R
authors.lastname: Saura
authors.forename: Minoru
authors.initials: M
authors.lastname: Doita
authors.forename: Masahiro
authors.initials: M
authors.lastname: Kurosaka
authors.forename: Kosaku
authors.initials: K
authors.lastname: Mizuno
mesh_terms: D000293:Adolescent; D000328:Adult; D002478:Cells, Cultured; D017077:Culture Media, Conditioned / Q000737:chemistry; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D015232:Dinoprostone / Q000032:analysis / Q000096:biosynthesis; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007150:Immunohistochemistry; D007405:Intervertebral Disc Displacement / Q000201:enzymology* / Q000209:etiology* / Q000473:pathology; D007527:Isoenzymes / Q000037:antagonists & inhibitors / Q000096:biosynthesis* / Q000235:genetics; D008159:Lumbar Vertebrae / Q000293:injuries / Q000473:pathology; D008161:Lumbosacral Region; D008297:Male; D008565:Membrane Proteins; D008875:Middle Aged; D009280:Naphthaleneacetic Acids / Q000494:pharmacology; D011451:Prostaglandin-Endoperoxide Synthases / Q000096:biosynthesis* / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016103:Spinal Fractures / Q000473:pathology
chemical_list: D017077:Culture Media, Conditioned; D004791:Enzyme Inhibitors; D007527:Isoenzymes; D008565:Membrane Proteins; D009280:Naphthaleneacetic Acids; D012333:RNA, Messenger; C044612:6-methoxy-2-naphthylacetic acid; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; C496511:PTGS1 protein, human; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone