Aim:To investigate the effects of the wingless-related MMTV integration site 3A(Wnt3a) signaling on the proliferation,migration,and the myogenic and adipogenicdifferentiation of rat bone marrow mesenchymal stem cells (rMSC).Methods:Primary MSC were isolated and cultured from Sprague-Dawley rats and character-ized by flow cytometry.Mouse L cells were transfected with Wnt3a cDNA,andconditioned media containing active Wnt3a proteins were prepared.Cell prolif-eration was evaluated by cell count and 5-bromodeoxyuridine incorporation assay.The migration of rMSC was performed by using a transwell migration and woundhealing assay.The myogenic and adipogenic differentiation in rMSC were exam-ined by light microscopy,immunofluorescence,and RT-PCR at different timepoints after myogenic or adipogenic introduction.Results:Wnt3a signaling in-duced β-catenin nuclear translocation and activated the Wnt pathway in rMSC.In the presence of Wnt3a,rMSC proliferated more rapidly than the control cells,keeping their differentiation potential.Moreover,Wnt3a signaling induced 2.62%and 3.76% of rMSC-expressed desmin and myosin heavy chain after being cul-tured in myogenic medium.The myogenic differentiation genes,including Pax7,MyoD,Myf5,Myf4,and myogenin,were activated after Wnt3a treatment.On theother hand,Wnt3a inhibited the adipogenic differentiation in rMSC through thedownregulated expression of CCAAT/enhancer-binding protein alpha (C/EBPalpha)and peroxisome proliferator-activated receptor gamma (PPARgamma).Furthermore,Wnt3a promoted the migration capacity of rMSC.Conclusion:The results indi-cate that Wnt3a signaling can induce myogenic differentiation in rMSC.Wnt3asignaling is also involved in the regulation of the proliferation and migration ofrMSC.These results could provide a rational foundation for cell-based tissuerepair in humans. Aim: To investigate the effects of the wingless-related MMTV integration site 3A (Wnt3a) signaling on the proliferation, migration, and the myogenic and adipogenic differentiation of rat bone marrow mesenchymal stem cells (rMSC). Methods: Primary MSC were isolated and cultured from Sprague-Dawley rats and character-ized by flow cytometry. Mouse L cells were transfected with Wnt3a cDNA, and conditioned media containing active Wnt3a proteins were prepared. Cell prolif-eration was evaluated by cell count and 5-bromodeoxyuridine incorporation assay. The migration of rMSC was performed by using a transwell migration and wound healing assay. myogenic and adipogenic differentiation in rMSC were examined-ined by light microscopy, immunofluorescence, and RT-PCR at different timepoints after myogenic or adipogenic introduction. Results: Wnt3a signaling in-duced β- catenin nuclear translocation and activated the Wnt pathway in rMSC. the presence of Wnt3a, rMSC proliferated more rapidly than the control cells, keep ing their differentiation potential. Moreover, Wnt3a signaling induced 2.62% and 3.76% of rMSC-expressed desmin and myosin heavy chain after being cultructed in myogenic medium. including Pax7, MyoD, Myf5, Myf4, and myogenin, were activated after Wnt3a treatment. On theother hand, Wnt3a inhibited the adipogenic differentiation in rMSCs through the downregulated expression of CCAAT / enhancer-binding protein alpha (C / EBPalpha) and peroxisome proliferator-activated receptor gamma (PPARgamma) capacity of rMSC.Conclusion: The results indi-cate that Wnt3a signaling can induce myogenic differentiation in rMSC. Wnt3 asignaling is also involved in the regulation of the proliferation and migration of rMSC. These results could provide a rational foundation for cell-based tissue repair in humans.