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  • Title: The Effects of Anti-TGF-β1 on Epithelial-Mesenchymal Transition in the Pathogenesis of Adenomyosis.
    Author: Kay N, Huang CY, Shiu LY, Yu YC, Chang Y, Suen JL, Tsai EM, Huang SJ.
    Journal: Reprod Sci; 2020 Sep; 27(9):1698-1706. PubMed ID: 32253735.
    Abstract:
    Adenomyosis is defined as the presence of endometrial glands and stroma in the myometrium. The mechanisms associated with the pathogenesis of adenomyosis remain unclear. Epithelial-mesenchymal transition (EMT) is characterized by losing cell polarity and cell-cell adhesion together with gaining migratory and invasive properties of stromal cells to become mesenchymal stem cells. Transforming growth factor-β1 (TGF-β1), an anti-inflammatory cytokine secreted by multiple cell types, plays a crucial role in embryogenesis and tissue homeostasis. The induction of EMT and ultimate fibrosis by TGF-β1 is suggested to play a critical role in the pathogenesis of adenomyosis. Thus, this study aims to demonstrate the occurrence of EMT in and the effects of anti-TGF-β1 on the pathogenesis of adenomyosis. ICR mice were fed with 1 μg/g body weight of tamoxifen (TAM) by in the first 4 postnatal days (PNDs). Subsequently, the right and left uterine horns were correspondingly injected with or without 10 μg of anti-TGF-β1 neutralizing antibody on PND42 followed by sacrifice on PND64. E-cadherin, vimentin, and α-smooth muscle actin (α-SMA) expression in the uteri was evaluated by qRT-PCR, Western blot, and immunohistochemistry. Clusters of endometrial glands and increased numbers of vimentin-positive stromal cells in the disrupted α-SMA-positive myometrium were observed in the uteri from TAM-treated mice. Numbers of stromal cells in the myometrium and the disrupted myometrial continuity were reduced by anti-TGF-β1. Moreover, uterine expression of E-cadherin and vimentin/α-SMA was increased and decreased by anti-TGF-β1 treatment, respectively. Anti-TGF-β1 successfully inhibits EMT and the development of adenomyosis in mouse uteri.
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