Concentration of osteoprotegerin (OPG) in peritoneal fluid is increased in women with endometriosis

Human Reproduction
Miyuki HaradaYuji Taketani

Abstract

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. 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. 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 co...Continue Reading

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Citations

Dec 17, 2009·Biomarkers : Biochemical Indicators of Exposure, Response, and Susceptibility to Chemicals·Zhen HouJiayin Liu
Jan 20, 2016·American Journal of Reproductive Immunology : AJRI·Ayumi TaguchiYutaka Osuga
Sep 2, 2005·American Journal of Reproductive Immunology : AJRI·Yuri TakemuraYuji Taketani
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Apr 17, 2015·Environmental Science & Technology·Steven J BaloghAkihide Tada
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Dec 5, 2017·Experimental and Therapeutic Medicine·Hong XiaoHongbo Zhao
Aug 26, 2009·Reproductive Medicine and Biology·Yutaka Osuga
Feb 9, 2006·Clinical Science·Ingunn Holen, Claire M Shipman

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis