Abstract:【Abstract】 Objective To investigate the mechanism of glycogen synthase kinase 3β(GSK3β)inhibition on the proliferation of aging endothelial progenitor cells(EPCs).Methods Mononuclear cells (MNCs) were isolated from bone marrow in aging Wister rats by density gradient centrifugation combined. EPCs were cultured and transduced with replication defective adenovirus vector expressing catalytically inactive glycogen synthase kinase 3β(GKS3βKM) or green fluorescent protein. EPCs proliferation was assessed by cells count and 3{4,5dimethylthiazol2yl}2,5diphenyltetrazolium bromide (MTT)assay. The cell cycle of EPCs was measured by fluorescenceactivated cell sorting (FACS). The expression of phosphorglycogen synthase kinase 3β(pGSK3β), βcatenin and cyclinD1 in EPCs were detected by western blot. Results GSK3β inhibition improved aging EPCs proliferation. Compared with control group, EPCs proliferation was enhanced in GKS3βKM gene transfection group (GSKi group). The number of EPCs was obviously increased in GSKi groups than that in control group. S phrase in cell cycle was increased in GSKi group in comparison with control group by FACS assay. The protein expression of pGSK3β,βcatenin and cyclinD1 were significantly higher than that in control group. Conclusion GSK3β inhibition could improve aging EPCs proliferation by activating Wnt signal pathway.