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

被引:16
作者
Harada, M [1 ]
Osuga, Y [1 ]
Hirata, T [1 ]
Hirota, Y [1 ]
Koga, K [1 ]
Yoshino, O [1 ]
Morimoto, C [1 ]
Fujiwara, T [1 ]
Momoeda, M [1 ]
Yano, T [1 ]
Tsutsumi, O [1 ]
Taketani, Y [1 ]
机构
[1] Univ Tokyo, Fac Med, Dept Obstet & Gynecol, Bunkyo Ku, Tokyo 1138655, Japan
关键词
D O I
10.1093/humrep/deh412
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
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.
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页码:2188 / 2191
页数:4
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