The mechanism of endometrial mesenchymal stem cells inhibition of endometrial fibrosis based on Wnt/β-catenin / 安徽医科大学学报

ABSTRACT

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.