Expression of Ah Receptor and Dioxin-Related Genes in Human Uterine Endometrium in Women with or without Endometriosis.

DOI Web Site PubMed 被引用文献2件
  • IGARASHI TOSHIO
    Department of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo
  • OSUGA YUTAKA
    Department of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo
  • TSUTSUMI OSAMU
    Department of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo Core Research for Evolutional Science and Technology CREST, Kawaguchi Center Building
  • MOMOEDA MIKIO
    Department of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo
  • ANDO KAYO
    Department of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo
  • MATSUMI HIROTAKA
    Department of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo
  • TAKAI YASUSHI
    Department of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo
  • OKAGAKI RYUGO
    Department of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo
  • HIROI HISAHIKO
    Department of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo
  • FUJIWARA TOSHIHIRO
    Department of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo
  • YANO TETSU
    Department of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo
  • TAKETANI YUJI
    Department of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo

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抄録

2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin (TCDD) has been suggested as a possibble etiologic factor for endometriosis, a condition in which endometrium-like tissues are present outside the uterus. The prevailing view pertaining to the origin of endometriotic cells is that they are from eutopic endometrial cells which regurgitate through fallopian tubes. In order to get insight into the possible involvement of TCDD in the pathogenesis of endometriosis, we suspected that TCDD may act differently on the endometrium with or without endometriosis. To address this, we examined the presence of messenger RNAs of arylhydrocarbon receptor (AhR), AhR nuclear translocator (Arnt) and two dioxin-responsive genes, cytochrome P-450 1B1 (CYP1B1) and downstream of tyrosine kinases (p62(dok)), in the endometrium of women with or without endometriosis using semi-quantitative reverse transcription-polymerase chain reaction. All the genes were expressed throughout the menstrual cycle. The expression level of p62(dok) was higher in the proliferative phase than in the secretory phase. In contrast, the expression levels of AhR, Arnt and CYP1B1 seemed to be constant during the cycle. In terms of the comparison between non-endometriosis and endometriosis group, the mRNA levels of AhR, Arnt, CYP1B1 and p62(dok) were essentially similar. Interestingly, AhR mRNA level was significantly lower in smokers than in non-smokers. Based on the regression analysis, significant linear and positive correlations were observed between AhR and Arnt mRNA levels, and between Arnt and p62(dok) mRNA levels. In summary, expression of AhR and dioxin-related genes in the endometrium did not differ in women with or without endometriosis.

収録刊行物

  • Endocrine Journal

    Endocrine Journal 46 (6), 765-772, 1999

    一般社団法人 日本内分泌学会

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