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Etiology matters - Comparing Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy (TBI – MBD-seq)

ABSTRACT: Explore DNA methylation in traumatic brain injury model of epilepsy and its relationship to gene expression. Examination of methylation changes in stimulated rats compared to sham operated animals in traumatic brain injury model of epilepsy.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Noora Puhakka

PROVIDER: E-GEOD-75119 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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

Dębski Konrad J KJ Pitkanen Asla A Puhakka Noora N Bot Anna M AM Khurana Ishant I Harikrishnan K N KN Ziemann Mark M Kaspi Antony A El-Osta Assam A El-Osta Assam A Lukasiuk Katarzyna K Kobow Katja K

Scientific reports 20160509

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 express ...[more]

PMID: 27157830

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Etiology matters - Comparing Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy (TBI â mRNA-seq)

Project description:Explore DNA methylation in traumatic brain injury model of epilepsy and its relationship to gene expression. Examination of expression changes in stimulated rats compared to sham operated animals in traumatic brain injury model of epilepsy.

2016-09-06 | E-GEOD-75120 | biostudies-arrayexpress

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

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Proteomics characterization of the neuroprotective effects of low-dose methamphetamine on rats with traumatic brain injury (TBI)

Project description:Traumatic brain injury (TBI) causes hospitalizations and mortality worldwide with no approved neuroprotective treatments available, partly due to a poor understanding of the molecular mechanisms underlying TBI neuropathology and neuroprotection. We previously reported that the administration of low-dose methamphetamine (MA) induced significant functional/cognitive improvements following severe TBI in rats. We further demonstrated that MA mediates neuroprotection in part, via dopamine-dependent activation of the PI3K-AKT pathway. Here, we further investigated the proteomic changes within the rat cortex and hippocampus following mild TBI (TM), severe TBI (TS), or severe TBI plus MA treatment (TSm) compared to sham operated controls (n=78 in total). We quantified >7,000 unique proteins in total and identified 402 and 801 altered proteins (APs) with high confidence in cortical and hippocampal tissues, respectively. The overall profile of APs observed in TSm rats more closely resembled those seen in TM rather than TS rats. Pathway analysis suggested beneficial roles for acute signaling through IL-6, TGFβ, and IL-1β. Moreover, changes in fibrinogen levels observed in TSm rats suggested a potential role for these proteins in reducing/preventing TBI-induced coagulopathies. These data facilitate further investigations to identify specific pathways and proteins that may serve as key targets for the development of neuroprotective therapies.

2021-03-02 | PXD024317 | Pride

Etiology matters - Comparing Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy (Amygdala stimulation â MBD-seq)

Project description:Explore DNA methylation in focal amygdala stimulation model of epilepsy and its relationship to gene expression. Examination of methylation changes in stimulated rats compared to sham operated animals in focal amygdala stimulation model of epilepsy.

2016-09-06 | E-GEOD-75400 | biostudies-arrayexpress

Etiology matters - Comparing Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy (Amygdala stimulation â mRNA-seq)

Project description:Explore DNA methylation in focal amygdala stimulation model of epilepsy and its relationship to gene expression. Examination of expression changes in stimulated rats compared to sham operated animals in focal amygdala stimulation model of epilpesy.

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Common molecular signature of two neuroprotective agents

Project description:The current lack of proven pharmacological treatment options for traumatic brain injury (TBI) patients reflects the poor translation of successful preclinical studies in clinical trials. This may be due to poor choice of therapeutic agents based on incomplete knowledge of critical elements of neuroprotection. Our goal is to expedite discovery and translation of therapeutic agents that can improve functional outcome by identifying the common molecular profile of neuroprotective drugs. Since damage to the hippocampus is associated with TBI-induced deficits in learning and memory, we analyzed of the hippocampal transcriptional profiles of TBI rats treated with two clinically used drugs metyrapone and carbenoxolone, which have been shown to improve cognitive deficits in previous studies. Despite their different structures, we found that MT and CB have similar effects on several known biological pathways. The neuroprotective effects of these drugs are associated with a distinctive molecular signature which is characterized not by changes in expression of any individual gene but by a common global effect on multiple cell signaling pathways. These data suggest that drug treatments that induce a coordinated attenuation of multiple injury-induced cell signaling networks, both deleterious and protective, have high translational potential. There were 16 samples for array analysis, two biological replicates each for control (4 and 24 hour), TBI (4 and 24 hour), TBI plus MT (4 and 24 hour) and TBI plus CB (4 and 24 hour). Each biological sample, which is a pooled RNA sample (laser captured CA3 pyramidal neurons) from the hippocampus of 3-6 rats, was hybridized to duplicate arrays so that there were 32 gene arrays in this study.

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Deep sequencing reveals increased DNA methylation in chronic rat epilepsy (mRNA-seq)

Project description:Explore DNA methylation in chronic epilepsy and its relationship to gene expression. Examination of expression changes in pilocarpine-treated rats compared to controls and pilocarpine-treated rats on a ketogenic diet.

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Proteomic analysis identifies plasma correlates of remote ischemic conditioning in the context of experimental traumatic brain injury

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2021-06-03 | PXD020420 | Pride

RNA-Sequencing of USP15 knock-out mice injected with kainate

Project description:Transcriptome studies of brain resections from mesial temporal lobe epilepsy (mTLE) patients revealed a dysregulation of transforming growth factor (TGF)-β, interferon (IFN)-α/β and nuclear factor erythroid 2-related factor 2 (NRF2) pathways among other neuroinflammatory mechanisms. Since ubiquitin-specific proteases (USP), in particular USP15, have been shown to regulate these pathways, we hypothesized that the blockade of USP15 may provide therapeutic relief in treatment-resistant epilepsies. The intrahippocampal kainate mouse model for mTLE, an established model for pharmacoresistant epilepsy was used for validation of USP15 as a therapeutic target. Transgenic mice which constitutively lack USP15 underwent intrahippocampal kainate injections to investigate the impact of USP15 inactivation at the transcriptomic level.

2023-10-12 | E-MTAB-12633 | biostudies-arrayexpress

RNA-Sequencing of USP15 conditional knock-out mice injected with kainate - dataset 2

Project description:Transcriptome studies of brain resections from mesial temporal lobe epilepsy (mTLE) patients revealed a dysregulation of transforming growth factor (TGF)-β, interferon (IFN)-α/β and nuclear factor erythroid 2-related factor 2 (NRF2) pathways among other neuroinflammatory mechanisms. Since ubiquitin-specific proteases (USP), in particular USP15, have been shown to regulate these pathways, we hypothesized that the blockade of USP15 may provide therapeutic relief in treatment-resistant epilepsies. The intrahippocampal kainate mouse model for mTLE, an established model for pharmacoresistant epilepsy was used for validation of USP15 as a therapeutic target. Transgenic mice which inducibly lack USP15 underwent intrahippocampal kainate injections to investigate the impact of USP15 downregulation at the transcriptomic level.

2023-10-12 | E-MTAB-12634 | biostudies-arrayexpress

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