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Etiology matters - genomic DNA methylation patterns in three rat models of acquired epilepsy

Dębski, Konrad J, Pitkanen, Asla, Puhakka, Noora, Bot, Anna M, Khurana, Ishant, Harikrishnan, KN, Ziemann, Mark, Kaspi, Antony, El-Osta, Assam, Lukasiuk, Katarzyna and Kobow, Katja 2016, Etiology matters - genomic DNA methylation patterns in three rat models of acquired epilepsy, Scientific reports, vol. 6, pp. 1-14, doi: 10.1038/srep25668.

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Title Etiology matters - genomic DNA methylation patterns in three rat models of acquired epilepsy
Author(s) Dębski, Konrad J
Pitkanen, Asla
Puhakka, Noora
Bot, Anna M
Khurana, Ishant
Harikrishnan, KN
Ziemann, MarkORCID iD for Ziemann, Mark orcid.org/0000-0002-7688-6974
Kaspi, Antony
El-Osta, Assam
Lukasiuk, Katarzyna
Kobow, Katja
Journal name Scientific reports
Volume number 6
Article ID 25668
Start page 1
End page 14
Total pages 14
Publisher Nature Publishing Group
Place of publication London, Eng.
Publication date 2016-05-09
ISSN 2045-2322
Keyword(s) cluster analysis
DNA methylation
disease models, animal
epilepsy
gene expression regulation
genome
molecular sequence annotation
nerve degeneration
RNA, messenger
epileptogenesis
etiology
gene expression
epileptogenic injury
focal amygdala stimulation
systemic pilocarpine injection
traumatic brain injury (TBI)
science & technology
Summary This study tested the hypothesis that acquired epileptogenesis is accompanied by DNA methylation changes independent of etiology. We investigated DNA methylation and gene expression in the hippocampal CA3/dentate gyrus fields at 3 months following epileptogenic injury in three experimental models of epilepsy: focal amygdala stimulation, systemic pilocarpine injection, or lateral fluid-percussion induced traumatic brain injury (TBI) in rats. In the models studies, DNA methylation and gene expression profiles distinguished controls from injured animals. We observed consistent increased methylation in gene bodies and hypomethylation at non-genic regions. We did not find a common methylation signature in all three different models and few regions common to any two models. Our data provide evidence that genome-wide alteration of DNA methylation signatures is a general pathomechanism associated with epileptogenesis and epilepsy in experimental animal models, but the broad pathophysiological differences between models (i.e. pilocarpine, amygdala stimulation, and post-TBI) are reflected in distinct etiology-dependent DNA methylation patterns.
Language eng
DOI 10.1038/srep25668
HERDC Research category C1.1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2016, Dębski, K. J. et al
Free to Read? Yes
Use Rights Creative Commons Attribution licence
Persistent URL http://hdl.handle.net/10536/DRO/DU:30113074

Document type: Journal Article
Collections: School of Life and Environmental Sciences
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.