Objective To explore the mechanism of mesenchymal epithelial transformation(EMT)mediated by Wnt/β-catenin signaling pathway in the inhibition of endometrial fibrosis by endometrial mesenchymal stem cells(eMSCs).Methods Eighteen female SD rats were randomly divided into Sham group,Model group and eMSCs group,with 6 rats in each group.Rats in Sham group merely had laparotomy without any treatment.A rat model of intrauterine adhesion(IUA)was established in the Model group and eMSCs group.In eMSCs group,the total a-mount of eMSCs cell suspension transplanted immediately after model injury was 0.05 ml(2×107 cells/ml)per u-terus for treatment.Three weeks later,the uterus with unilateral injury was collected for hematoxylin-eosin(HE)staining and Masson staining.Endometrial fibrosis,EMT,Wnt/β-catenin pathway protein expression were analyzed by protein blot.Results In the Model group,the structure of the uterine cavity was destroyed and the number of glands were significantly reduced with a large number of blue collagen fibers were accumulated.However,after eM-SCs treatment,the number of endometrial glands increased,and the fibrotic area decreased significantly.Compared with Sham group,the expression levels of type I collagen and α-SMA protein in Model group increased significantly(P<0.05),but decreased significantly in eMSCs group(P<0.05).In the Model group,the expressions of N-cadherin,vimentin and ZEB1 increased significantly,while the expression of E-cadherin decreased.However,in eMSCs group,the changes of protein of the above molecules were completely opposite.Compared with Sham group,the expression of β-catenin and C-myc increased in Model group(P<0.05).Compared with the Model group,the expressions of CyclinE,β-catenin and C-myc increased in eMSCs group(P<0.05).Conclusion eMSCs can promote endometrial repair in IUA rats by inhibiting EMT and endometrial fibrosis,which is partly achieved by ac-tivating Wnt/β-catenin signaling pathway.
万方数据
维普
