Table 4 Role of bivalent histone modifications in Osteo-/Odontogenic differentiation of bone/dental-derived MSCs
Epigenetic modification factors | Epigenetic marker | Cell | Function | Reference | |
|---|---|---|---|---|---|
Normal | MLL1 JMJD3 | H3K4me3↑ H3K27me3↓ | hDPCs | WNT5A is labeled by H3K4me3/H3K27me3 in the steady state, and the JMJD3 and MLL1 coactivator complexes mediate H3K27me3 resolution and initiation of transcription, ultimately regulating cell fate commitment in hDPCs | |
KDM7A/JHDM1D | H3K9me2↓ H3K27me2↓ | hDPSCs | SATB2 regulates DKK1 and KDM7A to modulate osteo-/odontogenic differentiation of hDPSCs through the Wnt/β-catenin signaling pathway | ||
NFIB-MLL1 KDM4B | H3K4me3↑ H3K9me3↓ | C3H10T1/2 | The NFIB-MLL1 complex mediated the deposition of H3K4me3 and resolution of H3K9me3 at the Dlx5 and Cebpa promoters and activated transcription of Runx2, Osx | ||
KDM2A | H3K36me2↓ H3K4me3↓ | SCAP | KDM2A catalyzes the demethylation of H3K4me3 and H3K36me2 in the EGER promoter and inhibits osteogenesis through interaction with the BCOR complex | ||
KDM2A | H3K36me2↓ H3K4me3↓ | SCAP | KDM2Ash promotes the transcription of the SFRP2 gene. SFRP2 enhances the osteo-/odontogenic differentiation potential of SCAP by activating OSX. | ||
Inflammatory and hypoxic conditions | KDM2A | H3K36me2↓ H3K4me3↓ | SCAP | KDM2A represses SFRP2 transcription and inhibits osteo-/odontogenic differentiation of SCAP. This repression is achieved by a reduction in the levels of H3K4me3 and H3K36me2 in the SFRP2 promoter region. | |
