Deciphering the Epigenetic Code of Stem Cells Derived From Dental Tissues

Ye Li,Dandan Pei,Xitong Zhao,Meng Sun,Ang Li

doi:10.3389/fdmed.2021.807046

Ye Li, Dandan Pei + Show 3 more

Open Access

https://doi.org/10.3389/fdmed.2021.807046

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Abstract

Stem cells derived from dental tissues (DSCs) exhibit multipotent regenerative potential in pioneering tissue engineering regimens. The multipotency of DSCs is critically regulated by an intricate range of factors, of which the epigenetic influence is considered vital. To gain a better understanding of how epigenetic alterations are involved in the DSC fate determination, the present review overviews the current knowledge relating to DSC epigenetic modifications, paying special attention to the landscape of epigenetic modifying agents as well as the related signaling pathways in DSC regulation. In addition, insights into the future opportunities of epigenetic targeted therapies mediated by DSCs are discussed to hold promise for the novel therapeutic interventions in future translational medicine.

Highlights

Dental stem cells (DSCs), a subgroup of mesenchymal stem cells (MSCs), are isolated mainly from dental pulp or periodontium-associated tissues
This study provided a new rationale to reveal the molecular mechanisms of the inflamed dental pulp and was of instructive significance in revealing the effect of DNMT1 on the differentiation capacity of dental pulp stem cells (DPSCs) in inflammatory conditions
Tao et al indicated that the coordinated expression of p300 and HDAC3 was critical for odontoblast differentiation of stem cells from apical papilla (SCAP), providing new hints for restorative dentistry [57]

Summary

Introduction

Dental stem cells (DSCs), a subgroup of mesenchymal stem cells (MSCs), are isolated mainly from dental pulp or periodontium-associated tissues. DNA methylation is vital to the regulation of osteogenic and odontoblastic differentiation of DSCs, contributing to the regeneration of bone-related defects. KDM5A inhibited the odontogenic differentiation potentiality of DPSCs by removing H3K4me3 from DMP1, DSPP, OSX, and OCN promoters [49].

Results

Conclusion