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

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/beta-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/beta-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 beta-catenin and Fzd2 mRNA expression. In addition, we observed a significant increase of nuclear beta-catenin in endometriotic lesions, a hallmark of Wnt/beta-catenin pathway activation. Stromal beta-catenin staining was found in 45.4% of endometrial tissues and 77.8% of endometriotic lesions. beta-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/beta-catenin components expression suggests an increased activity of this pathway in endometriosis.