Vitamin C and MEK Inhibitor PD0325901 Synergistically Promote Oligodendrocytes Generation by Promoting DNA Demethylation

Molecules. 2024 Dec 16;29(24):5939. doi: 10.3390/molecules29245939.

Abstract

DNA methylation and demethylation are key epigenetic events that regulate gene expression and cell fate. DNA demethylation via oxidation of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) is typically mediated by TET (ten-eleven translocation) enzymes. The 5hmC modification is considered an intermediate state of DNA demethylation; it is particularly prevalent in the brain and is believed to play a role in the development of many cell types in the brain. Our previous studies have identified that vitamin C (Vc) and MEK inhibitor PD0325901 could significantly promote OPC (oligodendrocyte progenitor cell)-to-OL (oligodendrocyte) differentiation. Here we discovered that Vc and PD0325901 may promote OPC-to-OL differentiation by inducing DNA demethylation via hydroxymethylation. Blocking 5hmC formation almost totally blocked Vc- and PD0325901-stimulated OPC-to-OL differentiation. In addition, TET1 is not involved in Vc,- and PD0325901-promoted OL generation. We also found a synergistic effect between the two compounds in inducing OL generation, suggesting the possibility of a combination therapy for demyelination diseases in the future.

Keywords: 5-hydroxymethylcytosine; DNA demethylation; PD0325901; TET enzymes; oligodendrocyte; oligodendrocyte progenitor cell; vitamin C.

MeSH terms

  • 5-Methylcytosine / analogs & derivatives
  • 5-Methylcytosine / metabolism
  • Animals
  • Ascorbic Acid* / pharmacology
  • Benzamides* / pharmacology
  • Cell Differentiation* / drug effects
  • DNA Demethylation* / drug effects
  • DNA Methylation / drug effects
  • Diphenylamine* / analogs & derivatives
  • Diphenylamine* / pharmacology
  • Drug Synergism*
  • Mice
  • Oligodendroglia* / drug effects
  • Oligodendroglia* / metabolism
  • Protein Kinase Inhibitors / pharmacology
  • Proto-Oncogene Proteins / antagonists & inhibitors
  • Proto-Oncogene Proteins / metabolism

Substances

  • Ascorbic Acid
  • mirdametinib
  • Diphenylamine
  • Benzamides
  • 5-Methylcytosine
  • Protein Kinase Inhibitors
  • 5-hydroxymethylcytosine
  • Proto-Oncogene Proteins