Conclusions
KDM1A might have different role in different stages of osteo/dentinogenic differentiation process by binding partner with PLOD2, and finally resulted in the inhibited function for the osteo/dentinogenesis in SCAPs. Our studies provided a further understanding of the regulatory mechanisms of dynamic osteo/dentinogenic differentiation process in dental tissue MSCs.
Material and methods
We obtained SCAPs from immature teeth. Alkaline phosphatase (ALP) activity assay, Alizarin red staining, quantitative calcium analysis, osteogenesis-related genes expression and in vivo transplantation experiment were used to explore the osteo/dentinogenic differentiation. Co-immunoprecipitation (Co-IP) assay was used to investigate the binding protein.
Methods
We obtained SCAPs from immature teeth. Alkaline phosphatase (ALP) activity assay, Alizarin red staining, quantitative calcium analysis, osteogenesis-related genes expression and in vivo transplantation experiment were used to explore the osteo/dentinogenic differentiation. Co-immunoprecipitation (Co-IP) assay was used to investigate the binding protein.
Results
Knock-down of KDM1A reduced ALP activity and mineralization, promoted the expressions of osteo/dentinogenic differentiation markers DSPP, DMP1, BSP and key transcript factors, RUNX2, OSX, DLX2 in SCAPs, and also enhanced the osteo/dentinogenesis in vivo. In addition, KDM1A could associate with PLOD2 to form protein complex. And knock-down of PLOD2 inhibited ALP activity and mineralization, and promoted the expressions of DSPP, DMP1, BSP, RUNX2, OSX and DLX2 in SCAPs. Conclusions: KDM1A might have different role in different stages of osteo/dentinogenic differentiation process by binding partner with PLOD2, and finally resulted in the inhibited function for the osteo/dentinogenesis in SCAPs. Our studies provided a further understanding of the regulatory mechanisms of dynamic osteo/dentinogenic differentiation process in dental tissue MSCs.