Dimethyloxalylglycine regulates osteogenesis of dental pulp stem cells through PI3K/AKT signaling pathways.

BACKGROUND

Dental pulp mesenchymal stem cells (DPSCs) are typically cultivated in vitro under normoxic conditions, which may adversely affect their biological functions during research and treatment. Dimethyloxalylglycine (DMOG) is a small-molecule drug that has demonstrated impressive therapeutic outcomes in conditions such as osteoporosis.

OBJECTIVE

However, the influence of DMOG on the osteogenesis associated with DPSCs remains inadequately understood. We propose that DMOG may significantly impact the biological functions related to osteogenesis in DPSCs when exposed to normoxic conditions.

MATERIALS AND

METHODS

DPSCs were obtained through tissue block enzyme digestion. Tube formation experiment was conducted, quantitative polymerase chain reaction (qPCR) was employed to assess the angiogenic activity of DPSCs. Additionally, alkaline phosphatase (ALP) activity tests, alizarin red staining (ARS), qPCR and western blotting (WB) assays were utilized to evaluate the osteogenic activity of DPSCs. The proposed mechanism was confirmed through repeated experiments.

RESULTS

DMOG significantly influences the osteogenic functions of DPSCs under normoxic conditions. Our findings further confirm that DMOG stimulates the phosphatidylinositol 3-kinase (PI3K)/Protein kinase B (AKT) signaling pathway in DPSCs via phosphorylation. Inhibition of this pathway can partially impede the biological effects of DPSCs related to osteogenesis and angiogenesis.

CONCLUSION

We have addressed the gap in understanding the effect of DMOG on the osteogenesis of DPSCs. Unlike previous studies that examined the regulation of osteogenesis in stem cells by DMOG, our findings suggest that a lower dose of DMOG is sufficient to enhance the osteogenesis of DPSCs. This could represent a promising strategy for cellular therapy in bone regeneration.