Table 3 Role of H3K27 histone methylation modification in Osteo-/Odontogenic differentiation of bone/dental-derived MSCs

From: Role and mechanisms of histone methylation in osteogenic/odontogenic differentiation of dental mesenchymal stem cells

Epigenetic modification factors

Epigenetic marker

Cell

Function

Reference

Normal

EZH2

H3K27me3↑

hDPCs

EZH2 inhibits the osteogenic differentiation and mineralization of hDPCs through the β-catenin pathway and promotes their proliferation

117

H3K27me3↑

PDLSCs

LncRNA SNHG1 increases the level of H3K27me3 at the KLF2 promoter through the action of EZH2, thereby repressing the expression of ALP, Osx, and OCN

120

H3K27me3↑

PDLSCs

LncRNAs SNHG8 and EZH2 reciprocally regulate each other to silence KLF transcription and inhibit osteogenic differentiation

120,121

H3K27me3↑

hDPCs

LncRNA CARMN promotes odontogenic differentiation of hDPCs by inhibiting the activity of EZH2

122

EZH2

KDM6A

H3K27me3

BM-MSCs

EZH2 and KDM6A co-regulate the expression of H3K27me3 in the promoter region of genes, thereby influencing the expression of Runx2, OPN, and OCN

137

EZH2

KDM6A/B

H3K27me3

hDFSCs

LncRNA HOTAIRM1 promotes DFSCs-mediated bone regeneration by regulating the HIF1α/KDM6/EZH2/H3K27me3 axis

127

KDM6B

H3K27me3↓

hDPCs

The transcription of downstream odontogenic marker genes, including OSX, BGLAP, and SPP1, is initiated

100,131

KDM6B

H3K27me3↓

hDPSCs

The miR-93-5p targets KDM6B and removes the H3K27me3 marker on the BMP2 promoter, thereby regulating the odontogenic differentiation and dentin formation of DPSCs

133

Inflammatory conditions

EZH2

H3K27me3↑

PDLSCs

Knockdown of EZH2 promotes osteogenic differentiation by inhibiting the TLR4/MyD88/NF-κB signaling pathway

118

KDM6B

H3K27me3↓

PDLSCs

KDM6B forms a protein complex with BCRO to inhibit IGFBP5 transcription. KDM6B removes H3K27me3 from the promoter region of the downstream gene IGFBP5 and mediates periodontal tissue regeneration

136