Di-san junyi daxue xuebao (Jun 2020)

Role of NF-κB signaling pathway in treatment of intrauterine adhesions by human amniotic mesenchymal stem cells

  • GOU Yating,
  • ZHANG Wenwen,
  • LI Changjiang,
  • YU Jie,
  • MAO Yanhua

DOI
https://doi.org/10.16016/j.1000-5404.202003065
Journal volume & issue
Vol. 42, no. 11
pp. 1101 – 1108

Abstract

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Objective To investigate the role of IκB-α/NF-κB signaling pathway in the treatment of intrauterine adhesions (IUA) by human amniotic mesenchymal stem cells (hAMSCs). Methods In vivo experiment: 18 SD female rats were randomly divided into Sham group, IUA model group and hAMSCs group. The number of endometrial glands and the percentage of fibrotic area were calculated by HE staining and Masson staining, respectively. Immunohistochemistry was used to detect the expression levels of IκB-α (NF-κB inhibitor), nuclear transfer factor P65, E-cadherin and vimentin in endometrial tissue. In vitro experiments: hAMSCs were induced by exogenous growth factors (10 ng/mL TGF-β1+EGF+PDGF-BB) and 10 nmol/L BAY11-7082 combined with above growth factors for 5 d, respectively, and the cells without treatment served as blank control. Fluorescence quantitative PCR was used to detect the expression levels of IκB-α, and cytokeratins CK-7 and CK-19. Results In vivo experiment: The expression levels of IκB-α, P65 and vimentin was significant higher, while that of E-cadherin was obviously lower in the model group than the Sham group (all P < 0.05); the expression levels of IκB-α, P65 and vimentin in the hAMSCs group were notably lower, while that of E-cadherin was higher than the model group (all P < 0.05). In vitro experiment: Compared with the control group, the expression of IκB-α was decreased but that of CK-7 was increased in the induction group; The expression levels of CK-7 and CK-19 were increased significantly in the inhibitor group than the induction group (both P < 0.05). Conclusion hAMSCs transplantation have therapeutic effect on uterine adhesions, which may be due to its promoting the transformation of hAMSCs into endometrial epithelial cells by inhibition of IκB-α/NF-κB pathway activation.

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