Proceedings of the Texas A&M Medical Student Grand Rounds

Dysregulation of DNA Methylation Profiles in Neural Stem Cells: A Consequence of Ethanol Exposure

August 10, 2017 Sasha Burrowes

Sasha Burrowes

Fetal Alcohol Syndrome (FAS) and Fetal Alcohol Spectrum Disorders (FASD) are leading non-genetic causes of neurodevelopmental disabilities in the US and worldwide1. Acting as a teratogen, ethanol has been shown to drastically change the developmental course of maturing neural stem cells in treated mouse NSCs via alterations in DNA methylation, histone modifications, and microRNA regulation.2,3,4 It has been previously shown, that alcohol does not kill fetal neural stem cells (NSCs), but instead, promotes aberrant maturation.2,3,4 However, the mechanisms underlying premature maturation and loss of renewal capacity are poorly understood. Investigation of ethanol-induced alterations in the epigenetic profiles of neural stem cells may further the development of necessary practices in education and crafting novel treatment interventions. METHODS To give a global epigenetic perspective, human embryonic stem cells were treated with ethanol, and RNA and genomic DNA were extracted. Changes in methylation of transcription start sites (TSS) and CpG islands were quantified as percent changes in DNA methylation, and pluripotent gene expression profiles were evaluated.5 In effort to further investigate neural specific targets of ethanol teratogenesis, Methyl CpG Binding protein 2 (Mecp2) was examined in murine neural stem cells (mNSCs). An ethanol treatment paradigm was utilized in cultured neurospheres to model binge and chronic ethanol exposure as well as withdrawal. Hydroxymethylated DNA immunoprecipitation (hMeDIP) and methylated DNA immunoprecipitation (MeDIP) reflected region specific changes in methylation on Mecp2 regulatory elements (REs). Additionally, DNA dot blot assays were used to identify global alterations in DNA methylation.6 RESULTS In hESCs despite each chromosome showing an overall increase in methylation status, a large number of gene promoters showed hypomethylation as a result of ethanol exposure.5 This indicates that the effects of ethanol exposure may result in widespread variance in the transcriptional regulation of hESC genes. DNA methylation analysis of Mecp2 gene loci in differentiating NSCs revealed increased 5-hydroxymethylcytosine (5hmC) and decreased 5-methylcytosine (5mC) enrichment at specific REs were associated with upregulated Mecp2/MeCP2 following continuous ethanol exposure. Withdrawal treatment showed significant hypermethylation, which corresponded to a significant decrease in Mecp2 transcript and protein.6 CONCLUSION A combination of ethanol induced epigenetic dysregulation during exposure and withdrawal may potentiate alterations in patterns of neural maturation and differentiation leading to FAS neuropathology. Investigation of epigenetic modulation of Mecp2 gene loci may not only give valuable insight into a mechanism of ethanol teratogenesis, but also a potential avenue for novel treatment of FAS in the future.

  1. Lunde ER, Washburn SE, Golding MC, Bake S, Miranda RC, Ramadoss J. Alcohol-Induced Developmental Origins of Adult-Onset Diseases. Alcoholism: Clinical and Experimental Research. 2016;40(7):1403-1414. doi:10.1111/acer.13114.
  2. Veazey KJ, Carnahan MN, Muller D, Miranda RC, Golding MC. Alcohol-Induced Epigenetic Alterations to Developmentally Crucial Genes Regulating Neural Stemness and Differentiation. Alcoholism: Clinical and Experimental Research. 2013;37(7):1111-1122. doi:10.1111/acer.12080.
  3. Resendiz M, Mason S, Lo C-L, Zhou FC. Epigenetic regulation of the neural transcriptome and alcohol interference during development. Frontiers in Genetics. 2014;5. doi:10.3389/fgene.2014.00285.
  4. Kleiber ML, Diehl EJ, Laufer BI, et al. Long-term genomic and epigenomic dysregulation as a consequence of prenatal alcohol exposure: a model for fetal alcohol spectrum disorders.Frontiers in Genetics. 2014;5. doi:10.3389/fgene.2014.00161.
  5. Khalid O, Kim JJ, Kim H-S, et al. Gene expression signatures affected by alcohol-induced DNA methylomic deregulation in human embryonic stem cells. Stem cell research. 2014;12(3):791-806. doi:10.1016/j.scr.2014.03.009.
  6. Liyanage V, Zachariah R, Davie J, Rastegar M. Ethanol deregulates Mecp2/MeCP2 in differentiating neural stem cells via interplay between 5-methylcytosine and 5-hydroxymethylcytosine at the Mecp2 regulatory elements. Experimental Neurology. 2015;265:102-117. doi:10.1016/j.expneurol.2015.01.006.

 

 

 

 

 

 

 

 

 

 

 

 

Neuroscience
Previous Post

SCFAs Pathologic Role in the Intestinal Microbiome and Autism

Next Post

Using mechanical stimuli to induce stem cell differentiation towards endothelial and smooth muscle cells for use in vascular grafts

Scientific Editors

Steve A. Maxwell

Executive Editor
Tel: 979-436-0804
smaxwell@medicine.tamhsc.edu

Robin Fuchs-Young

Deputy Editor
Tel: 979-845-5109
fuchs-young@medicine.tamhsc.edu
Administrative Editor

Janis Chmiel

Tel: 979-436-0856
chmiel@medicine.tamhsc.edu
Editorial Office
Tel.: 979-845-2726
Fax: 979-847-9481
chmiel@medicine.tamhsc.edu
Archives
  • July 2026
  • October 2025
  • September 2025
  • August 2025
  • July 2025
  • May 2025
  • September 2024
  • August 2024
  • July 2024
  • June 2024
  • May 2024
  • November 2023
  • September 2023
  • August 2023
  • July 2023
  • June 2023
  • August 2022
  • June 2022
  • May 2022
  • August 2021
  • July 2021
  • April 2021
  • October 2020
  • August 2020
  • July 2020
  • August 2019
  • July 2019
  • February 2019
  • July 2018
  • November 2017
  • October 2017
  • September 2017
  • August 2017
  • July 2017
  • January 2017
Proudly powered by WordPress | Theme: Fmi by Forrss.