| Background:Peritoneal fibrosis can lead to peritoneal ultrafiltration failure.Peritoneal dialysis (PD) for patients with end stage renal disease (ESRD) is seriouslylimited by ultrafiltration failure due to chronic peritoneal fibrosis which bring muchtrouble to patients.Peritoneal mesothelial cells (PMCs) is important in the maintenanceof peritoneal homeostasis, including transport and movement of fluid and particulatematerial, and the control of inflammation,.injury repair. PMCs may undertakeepithelial-myofibroblast transdifferentiation (EMT) to initiate the process of fibrosisbecause of the chronic injury.Bone mesenchymal stem cells (MSCs) are efficient forrepairing injuries and reducing fibrosis. MSCs mediate their therapeutic effects byeither differentiating into functional reparative cells or by secreting paracrine factorsthat are anti-inflammatory and anti-fibrogenic.Objective: This study was designed to investigate the effects of MSCs on EMTof PMCs induced by high-glucose peritoneal dialysis fluid.Methods: The EMT model of primary rat peritoneal mesothelial cells wasinduced by peritoneal dialysis fluid.The E-Cadherin/α-SMA/snail1expresstion ofperitoneal mesothelial cells were evaluated by light microscope andimmunofluorescence microscopy and western.Results:When cultured in peritoneal dialysis fluid medium,the E-Cadherinexpresstion was reduced and the α-SMA/snail expresstion was increased.Mesenchymal Stem Cells can attenuate E-Cadherin up-regulation andα-SMA/snail1up-regulation.Conclusion: MSCs can attenuate the EMT of primary rat peritoneal mesothelialcells induced by peritoneal dialysis fluid. |