From OPC to Oligodendrocyte: An Epigenetic Journey

Assia Tiane, Melissa Schepers, Ben Rombaut, Raymond Hupperts, Jos Prickaerts, Niels Hellings, Daniel van den Hove, Tim Vanmierlo*

*Corresponding author for this work

Research output: Contribution to journal(Systematic) Review article peer-review

35 Citations (Web of Science)

Abstract

Oligodendrocytes provide metabolic and functional support to neuronal cells, rendering them key players in the functioning of the central nervous system. Oligodendrocytes need to be newly formed from a pool of oligodendrocyte precursor cells (OPCs). The differentiation of OPCs into mature and myelinating cells is a multistep process, tightly controlled by spatiotemporal activation and repression of specific growth and transcription factors. While oligodendrocyte turnover is rather slow under physiological conditions, a disruption in this balanced differentiation process, for example in case of a differentiation block, could have devastating consequences during ageing and in pathological conditions, such as multiple sclerosis. Over the recent years, increasing evidence has shown that epigenetic mechanisms, such as DNA methylation, histone modifications, and microRNAs, are major contributors to OPC differentiation. In this review, we discuss how these epigenetic mechanisms orchestrate and influence oligodendrocyte maturation. These insights are a crucial starting point for studies that aim to identify the contribution of epigenetics in demyelinating diseases and may thus provide new therapeutic targets to induce myelin repair in the long run.

Original languageEnglish
Article number1236
Number of pages19
JournalCells
Volume8
Issue number10
DOIs
Publication statusPublished - Oct 2019

Keywords

  • oligodendrocyte
  • epigenetics
  • myelination
  • DNA METHYLTRANSFERASE INHIBITORS
  • HISTONE DEACETYLASE ACTIVITY
  • MULTIPLE-SCLEROSIS
  • PROGENITOR CELLS
  • WHITE-MATTER
  • GENE-EXPRESSION
  • ALZHEIMERS-DISEASE
  • PARKINSONS-DISEASE
  • DOWN-REGULATION
  • DIFFERENTIATION

Cite this