title: Concentration of osteoprotegerin (OPG) in peritoneal fluid is increased in women with endometriosis.
abstract: BACKGROUND
  Failure of apoptosis of refluxed endometrial cells within the peritoneal cavity is a possible etiologic factor for development of endometriosis. Osteoprotegerin (OPG) is a survival factor that exerts its effect by binding to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), thus preventing TRAIL from binding to the apoptosis receptors DR4 and DR5. In the present study, we addressed the possibility that the TRAIL/OPG system is involved in the pathogenesis of endometriosis.
  
  
  METHODS
  Concentrations of OPG and TRAIL in the peritoneal fluid (PF) of women with or without endometriosis were measured using specific enzyme-linked immunoabsorbent assay. The expression of DR4 and DR5 in the endometriotic tissue was examined by reverse transcription-polymerase chain reaction.
  
  
  RESULTS
  OPG concentrations in PF of women with endometriosis were significantly higher than those of women without endometriosis (P=0.006). With respect to the stages of the disease, the concentrations of OPG in women with stage III/IV endometriosis were significantly higher than in those without endometriosis and those with stage I/II endometriosis. On the other hand, the ratios of TRAIL/OPG concentrations were significantly lower in stage III/IV endometriosis compared to those in non-endometriosis and stage I/II endometriosis. DR5 mRNA expression was clearly detected in all the endometriotic tissues studied.
  
  
  CONCLUSIONS
  These findings suggest that the TRAIL/OPG system is involved in the pathophysiology of endometriosis, possibly affecting the apoptosis of endometriotic cells.
authors.affiliation: Department of Obstetrics and Gynecology, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
authors.forename: Miyuki
authors.initials: M
authors.lastname: Harada
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Osuga
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Hirata
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Hirota
authors.forename: Kaori
authors.initials: K
authors.lastname: Koga
authors.forename: Osamu
authors.initials: O
authors.lastname: Yoshino
authors.forename: Chieko
authors.initials: C
authors.lastname: Morimoto
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Fujiwara
authors.forename: Mikio
authors.initials: M
authors.lastname: Momoeda
authors.forename: Tetsu
authors.initials: T
authors.lastname: Yano
authors.forename: Osamu
authors.initials: O
authors.lastname: Tsutsumi
authors.forename: Yuji
authors.initials: Y
authors.lastname: Taketani
mesh_terms: D000328:Adult; D051017:Apoptosis Regulatory Proteins; D001202:Ascitic Fluid / Q000378:metabolism*; D016022:Case-Control Studies; D004715:Endometriosis / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006023:Glycoproteins / Q000378:metabolism*; D006801:Humans; D007247:Infertility, Female / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000378:metabolism; D009994:Osmolar Concentration; D053244:Osteoprotegerin; D012333:RNA, Messenger / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism*; D053220:Receptors, TNF-Related Apoptosis-Inducing Ligand; D018124:Receptors, Tumor Necrosis Factor / Q000235:genetics; D053221:TNF-Related Apoptosis-Inducing Ligand; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D051017:Apoptosis Regulatory Proteins; D006023:Glycoproteins; D008562:Membrane Glycoproteins; D053244:Osteoprotegerin; D012333:RNA, Messenger; D018160:Receptors, Cytoplasmic and Nuclear; D053220:Receptors, TNF-Related Apoptosis-Inducing Ligand; D018124:Receptors, Tumor Necrosis Factor; D053221:TNF-Related Apoptosis-Inducing Ligand; C505639:TNFRSF10B protein, human; C506030:TNFRSF11B protein, human; C505653:TNFSF10 protein, human; D014409:Tumor Necrosis Factor-alpha