Epigenetic Regulation of WNT3A Enhancer during Regeneration of Injured Cortical Neurons

Int J Mol Sci. 2020 Mar 10;21(5):1891. doi: 10.3390/ijms21051891.

Abstract

Traumatic brain injury is known to reprogram the epigenome. Chromatin immunoprecipitation-sequencing of histone H3 lysine 27 acetylation (H3K27ac) and tri-methylation of histone H3 at lysine 4 (H3K4me3) marks was performed to address the transcriptional regulation of candidate regeneration-associated genes. In this study, we identify a novel enhancer region for induced WNT3A transcription during regeneration of injured cortical neurons. We further demonstrated an increased mono-methylation of histone H3 at lysine 4 (H3K4me1) modification at this enhancer concomitant with a topological interaction between sub-regions of this enhancer and with promoter of WNT3A gene. Together, this study reports a novel mechanism for WNT3A gene transcription and reveals a potential therapeutic intervention for neuronal regeneration.

Keywords: WNT3A; enhancer regulation; epigenome; histone modification; neuronal regeneration; transcriptional regulation.

MeSH terms

  • Acetylation
  • Animals
  • Brain Injuries, Traumatic / genetics*
  • Brain Injuries, Traumatic / metabolism
  • Chromatin Immunoprecipitation
  • Disease Models, Animal
  • Enhancer Elements, Genetic
  • Epigenesis, Genetic
  • Histones / metabolism*
  • Methylation
  • Neurons / metabolism
  • Neurons / physiology*
  • Promoter Regions, Genetic
  • Rats
  • Rats, Sprague-Dawley
  • Regeneration
  • Wnt3A Protein / genetics*

Substances

  • Histones
  • Wnt3A Protein