DNMT1 Inhibitor Restores RUNX2 Expression and Mineralization in Periodontal Ligament Cells

Periodontal ligament cells (PDLCs) have well documented osteogenic potential; however, this commitment can be highly heterogenous, limiting their applications in tissue regeneration. In study, we use PDLC populations characterized by high and low potential (h-PDLCs l-PDLCs, respectively) to identify possible sources of such heterogeneity investigate whether the differentiation enhanced epigenetic modulation. h-PDLCs, basal expression levels pluripotency markers (NANOG, OCT4), DNA methyltransferases (DNMT1, DNMT3B), enzymes involved active demethylation (TET1, TET3) were prerequisite potential. Furthermore, these genes downregulated upon early osteogenesis, possibly allowing for increase key transcription factors, Runt-related factor 2 (RUNX2) SP7, ultimately, mineral nodule formation. l-PDLCs appeared locked multipotent state was further stimulation, correlating with RUNX2 impaired mineralization. Further upregulation DNMTs also evident, while pretreatment RG108, DNMTs' inhibitor, program through downregulation DNMTs, increased nuclear localization, accelerated markers, These findings point toward role Ten Eleven Translocations (TETs) support application approaches modulate biomineralization PDLCs.