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Related Experiment Video

Updated: Jul 29, 2025

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Characterisation of miRNA Expression in Dental Pulp Cells during Epigenetically-Driven Reparative Processes.

Michaela Kearney1, Paul R Cooper2, Anthony J Smith3

  • 1Division of Restorative Dentistry & Periodontology, Dublin Dental University Hospital, Trinity College Dublin, University of Dublin, D02 F859 Dublin, Ireland.

International Journal of Molecular Sciences
|May 27, 2023
PubMed
Summary

Next-generation biomaterials harness epigenetic machinery, including microRNAs (miRNAs) and epigenetic modifiers, to stimulate dental pulp cell repair and mineralization. This study reveals dynamic interactions between miRNAs and epigenetic drugs during this process.

Keywords:
DNA methyltransferase inhibitorRNA sequencingdental pulp stem cellsepigeneticshistone deacetylase inhibitormicroRNAnon-coding RNAvital pulp treatment

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Area of Science:

  • Regenerative Endodontics
  • Biomaterials Science
  • Molecular Biology

Background:

  • Regenerative endodontics aims to develop advanced biomaterials targeting epigenetic mechanisms like miRNAs, histone acetylation, and DNA methylation for pulp repair.
  • Histone deacetylase inhibitors (HDACi) and DNA methyltransferase inhibitors (DNMTi) promote mineralization in dental pulp cells (DPCs), but their interplay with miRNAs during this process remains unclear.

Purpose of the Study:

  • To profile miRNA expression during DPC mineralization.
  • To investigate the effects of HDACi (SAHA) and DNMTi (5-AZA-CdR) on miRNA expression, DPC mineralization, and proliferation.
  • To elucidate the interaction between miRNAs and epigenetic modifiers in DPC reparative processes.

Main Methods:

  • Small RNA sequencing and bioinformatic analysis to establish miRNA expression profiles.
  • Treatment of DPCs with SAHA and 5-AZA-CdR to assess effects on mineralization, proliferation, and miRNA expression.
  • Quantitative reverse transcription PCR (qRT-PCR) to validate miRNA expression changes.

Main Results:

  • Both SAHA and 5-AZA-CdR enhanced DPC mineralization but reduced cell proliferation.
  • Epigenetic modification led to widespread changes in miRNA expression, with identified miRNAs potentially regulating Wnt and MAPK pathways.
  • qRT-PCR confirmed differential regulation of selected miRNAs in response to epigenetic inhibitors during DPC mineralization.

Conclusions:

  • Epigenetic drug treatment induces mineralization in DPCs, accompanied by significant alterations in miRNA expression.
  • A dynamic interplay exists between miRNAs and epigenetic modifiers during DPC reparative processes, offering potential for targeted regenerative therapies.
  • These findings highlight the role of miRNAs in mediating epigenetic effects on DPC mineralization and differentiation.