Effect of human umbilical cord mesenchymal stem cells on proliferation and apoptosis of ectopic endometrial cells
Wang Chun-mei
Li Jie
Sun Wen-ping
Wu De-hui
Abstract：BACKGROUND:Mesenchymal stem cels can secrete a variety of cytokines and growth factors that promote the survival of surrounding cels and play a paracrine role. OBJECTIVE:To investigate the effect of human umbilical cord mesenchymal stem cels on the proliferation and apoptosis of ectopic endometrial cels. METHODS:After isolation and culture, human umbilical cord mesenchymal stem cels and ectopic endometrial cels were co-cultured as observation group, and ectopic endometrial cels cultured alone served as control group. At 24, 48, 72 hours of culture, the proliferation and apoptosis of ectopic endometrial cels were detected by MTT and flow cytometry, respectively; RT-PCR was used to measure the expression ofPTEN gene in ectopic endometrial cels. RESULTS AND CONCLUSION:At 24, 48 and 72 hours, the proliferation of ectopic endometrial cels in the observation was inhibited significantly as compared with the control group, and the hypodiploid peak ratio also increased significantly (P < 0.05). Over time, the cel inhibition rate was gradualy declined, and there were significant differences at different time points (alP < 0.05). Compared with the control group, the expression of PTEN gene was up-regulated significantly in the observation group (P < 0.05). In the observation group, the expression ofPTEN gene at 48 and 72 hours was significantly higher than that at 24 hours (P < 0.05). These findings indicate that in the human umbilical cord mesenchymal stem cels can inhibit the proliferation of ectopic endometrial celsin vitro and promote their apoptosis by up-regulation ofPTEN mRNA expression.
Keywords：Umbilical CordMesenchymal Stem CelsEndometriosisCoculture TechniquesPTEN PhosphohydrolaseCel ProliferationApoptosisTissue Engineering
Publication Date：2015-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：5( 6628-6632 )