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Aberrant levels of Wnt/β-catenin pathway components in a rat model of endometriosis

    1. [1] National Cancer Institute

      National Cancer Institute

      Estados Unidos

    2. [2] Universidade Federal do Rio de Janeiro

      Universidade Federal do Rio de Janeiro

      Brasil

    3. [3] Universidade Do Porto

      Universidade Do Porto

      Santo Ildefonso, Portugal

    4. [4] State University of East Zone, Rio de Janeiro, Brazil
  • Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 31, Nº. 8, 2016, págs. 933-942
  • Idioma: inglés
  • Enlaces
  • Resumen
    • Endometriosis is a benign gynecological disease affecting approximately 10-15% of women of reproductive age and 25-50% of all infertile women. It is characterized by the presence of glands and/or endometrial stroma outside the uterine cavity. Angiogenesis is a crucial process for the development and maintenance of endometriotic lesions. The Wnt/β-catenin pathway is a major promoter of angiogenesis in both physiological and pathological conditions. In the present study, we evaluated the expression of molecules related to the Wnt/β-catenin pathway in a rat model of peritoneal endometriosis. mRNA analyses showed significantly increased expression of Wnt4 and Wnt7b and decreased expression of Gsk3beta and E-cadherin in endometriotic lesions. However, there were no differences in β-catenin and Fzd2 mRNA expression. In addition, we observed a significant increase of nuclear β-catenin in endometriotic lesions, a hallmark of Wnt/ β -catenin pathway activation. Stromal β-catenin staining was found in 45.4% of endometrial tissues and 77.8% of endometriotic lesions. β-catenin nuclear localization was found in 18.2% of the endometrial tissues and 33.3% of endometriotic lesions. Finally, the expression of galectin-3, a regulator of this pathway, was increased in endometriosis. In summary, this pattern of Wnt/β-catenin components expression suggests an increased activity of this pathway in endometriosis.


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