Etiology matters – Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy

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...

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Published in:Scientific reports 2016-05, Vol.6 (1), p.25668-25668, Article 25668
Main Authors: Dębski, Konrad J., Pitkanen, Asla, Puhakka, Noora, Bot, Anna M., Khurana, Ishant, Harikrishnan, KN, Ziemann, Mark, Kaspi, Antony, El-Osta, Assam, Lukasiuk, Katarzyna, Kobow, Katja
Format: Article
Language:English
Subjects:
38/23
38/90
38/91
631/337/176
631/378/116
Amygdala
Animal models
Animals
Cluster Analysis
Dentate gyrus
Deoxyribonucleic acid
Disease Models, Animal
DNA
DNA methylation
DNA Methylation - genetics
Epilepsy
Epilepsy - genetics
Epilepsy - pathology
Etiology
Gene expression
Gene Expression Regulation
Genome
Genomes
Hippocampus
Humanities and Social Sciences
Male
Molecular Sequence Annotation
multidisciplinary
Nerve Degeneration - genetics
Nerve Degeneration - pathology
Pilocarpine
Rats, Sprague-Dawley
RNA, Messenger - genetics
RNA, Messenger - metabolism
Science
Traumatic brain injury
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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.
ISSN:2045-2322
2045-2322
DOI:10.1038/srep25668