Table 2 Role of H3K9 histone methylation modifications in Osteo-/Odontogenic differentiation of bone/dental-derived MSCs
Epigenetic modification factors | Epigenetic marker | Cell | Function | Reference | |
|---|---|---|---|---|---|
Normal | G9a | H3K9- H3K9me2 | hDP-MSCs | G9a facilitates the generation of H3K9me2 and suppresses the transcription of osteogenic markers, including Runx2, Ocn, and DSP. | |
Suv39h1 | H3K9- H3K9me2/3 | DPSCs | Suv39h1 forms a protein complex with Lhx8, which functions to inhibit the expression of odontogenic genes through the di/trimethylation of H3K9. | ||
KDM4B | H3K9me3 | hSCAP | DLX5 interacts with KDM4B and facilitates osteo-/odontogenic differentiation through the upregulation of OSX. | ||
H3K9me3 | DMSC | The P75NRT-mediated NGF signaling pathway induces the activation of the JNK cascade and KDM4B expression through the removal of inhibitory H3K9me3 marks, thereby stimulating DLX5 and subsequently promoting osteogenic differentiation. | |||
KDM4D | H3K9me2/3 | hSCAP | The combination of KDM4D and RPS5 promotes osteo-/odontogenic differentiation and the migration capacity of SCAP | ||
KDM3B | H3K9me2 | hSCAP | KDM3B upregulates the expression of Runx2, Osx, Ocn, and Dspp genes, thereby promoting osteo-/odontogenic differentiation in SCAP. | ||
