Wnt-GSK3β/β-Catenin Regulates the Differentiation of Dental Pulp Stem Cells into Bladder Smooth Muscle Cells

Figure 7

Wnt/GSK3β/β-catenin activation. 1: in the absence of canonical Wnt signaling, β-catenin is complexed with GSK3β, APC, and Axin, which facilitate the phosphorylation and subsequent degradation of β-catenin. 2: activation of canonical Wnt signaling by the growth factor, TGF-β1, and CM from SMC triggers phosphorylation of GSK3β, thereby disrupting the APC/Axin/GSK3β/β-catenin complex. 3: β-catenin which dissociates from the APC/Axin/GSK3β complex escapes from degradation and accumulates in the cytoplasm. 4: the stabilization and accumulation of β-catenin translocates into the nucleus and enhances the expression of growth factors, including TGF-β1, HGF, VEGF, and PDGF-BB, thus promoting the SMC differentiation from the DPSC clone A32. 5: Wnt/β-catenin signaling inhibitor, XAV939, and GSK3 inhibitors, SB216763 and LiCl, were used to block the Wnt/GSK3β/β-catenin signaling.