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NRSF mediated epigenetic mechanisms of ion channel dysfunction in experimental temporal lobe epilepsy [Control vs. Kainate, NRSE ODNs]

ABSTRACT: Oligodeoxynucleotides used to prevent NRSF binding to NRSE containing genes were utilized to prevent many kainate induced status epilepticus changes in gene expression.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE22894 | GEO | 2014/08/12

SECONDARY ACCESSION(S): PRJNA129121

REPOSITORIES: GEO

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NRSF mediated epigenetic mechanisms of ion channel dysfunction in experimental temporal lobe epilepsy [Kainate, NRSE ODNs vs. Kainate, scrambled ODNs]

Project description:Oligodeoxynucleotides used to prevent NRSF binding to NRSE containing genes were used to prevent many kainate induced status epilepticus changes in gene expression. Total RNA recovered from CA1 of hippocampus of rats receiving scrambled or NRSE oligodeoxynucleotides, and kainate injections (induced status epilepticus)

2014-08-12 | E-GEOD-22897 | biostudies-arrayexpress

NRSF mediated epigenetic mechanisms of ion channel dysfunction in experimental temporal lobe epilepsy [Kainate, NRSE ODNs vs. Kainate, scrambled ODNs]

Project description:Oligodeoxynucleotides used to prevent NRSF binding to NRSE containing genes were used to prevent many kainate induced status epilepticus changes in gene expression.

2014-08-12 | GSE22897 | GEO

NRSF mediated epigenetic mechanisms of ion channel dysfunction in experimental temporal lobe epilepsy [Control vs. Kainate, scrambled ODNs]

Project description:Oligodeoxynucleotides used to prevent NRSF binding to NRSE containing genes were utilized to prevent many kainate induced status epilepticus changes in gene expression.

2014-08-12 | GSE22896 | GEO

NRSF mediated epigenetic mechanisms of ion channel dysfunction in experimental temporal lobe epilepsy [Control vs. Kainate, NRSE ODNs]

Project description:Oligodeoxynucleotides used to prevent NRSF binding to NRSE containing genes were utilized to prevent many kainate induced status epilepticus changes in gene expression. Total RNA recovered from CA1 of hippocampus of rats receiving scrambled or NRSE oligodeoxynucleotides, and saline(controls) or kainate injections (induced status epilepticus)

2014-08-12 | E-GEOD-22894 | biostudies-arrayexpress

NRSF mediated epigenetic mechanisms of ion channel dysfunction in experimental temporal lobe epilepsy [Control vs. Kainate, scrambled ODNs]

Project description:Oligodeoxynucleotides used to prevent NRSF binding to NRSE containing genes were utilized to prevent many kainate induced status epilepticus changes in gene expression. Total RNA recovered from CA1 of hippocampus of rats receiving scrambled, and saline(controls) or kainate injections (induced status epilepticus)

2014-08-12 | E-GEOD-22896 | biostudies-arrayexpress

NRSF mediated epigenetic mechanisms of ion channel dysfunction in experimental temporal lobe epilepsy

Project description:This SuperSeries is composed of the SubSeries listed below.

2014-08-12 | GSE22899 | GEO

NRSF mediated epigenetic mechanisms of ion channel dysfunction in experimental temporal lobe epilepsy

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

2014-08-12 | E-GEOD-22899 | biostudies-arrayexpress

Impact of NRSF variant over-expression in SK-N-AS human neuroblastoma cells

2010-07-01 | GSE22467 | GEO

Impact of NRSF variant over-expression in SK-N-AS human neuroblastoma cells

Project description:Neuron-restrictive silencer factor (NRSF) and its isoforms are differentially regulated in rodent models of self-sustaining status epilepticus (SSSE). NRSF isoforms regulate genes associated with SSSE, including the proconvulsant tachykinins, brain-derived neurotrophic factor and multiple ion channels. NRSF isoforms may direct distinct gene expression patterns during SSSE and the ratio of each isoform may be a causative factor in traumatic damage to the CNS. Here we analysed global gene expression changes by microarray in human SK-N-AS neuroblastoma cells following the over expression of NRSF and a truncated isoform, HZ4. We used bioinformatics software to analyse the microarray dataset and correlated these data with epilepsy candidate gene pathways. Findings were validated by RT-PCR. We demonstrated that NRSF and HZ4 direct overlapping as well as distinct gene expression patterns and that they differentially modulated gene expression patterns associated with epilepsy. Finally we revealed that NRSF gene expression may be modulated by the anticonvulsant, phenytoin. This study provides fundamental information on networks of genes that may be altered during SSSE, following altered NRSF expression, which may be important in future therapeutic research and clinical analysis of genetic variation predisposing to epilepsy. Human SK-N-AS cells were treated with expression constructs over-expressing either the full length human transcription factor, NRSF, (via the RE-EX1 construct) or a truncated variant (via the HZ4 construct). Cells were treated for either 0hrs (base line controls), 24hrs or 48hrs, before being immediately processed for RNA extraction. An affymetrix microarray was employed to investigate gene expression patterns, comparing each time point (24hrs or 48hrs) againsts its baseline ()hrs) control. This experiment was performed in triplicate samples per batch, and over three batches.

2010-07-30 | E-GEOD-22467 | biostudies-arrayexpress

Proteomic profile of mouse hippocampus following kainate-induced epileptogenesis C4PR_LIV

Project description:Anti-epileptogenic agents that prevent the development of epilepsy following a brain insult remain the holy grail of epilepsy therapeutics. In order to identify such drugs, it is necessary to first understand the cellular and molecular events that underlie the epileptogenic process, from initial insult to the onset of spontaneous recurrent seizures. We have employed a label-free proteomic approach that allows quantification of large numbers of brain-expressed proteins in a single analysis in the well-established kainate (KA) mouse (C57BL/6J) model of epileptogenesis. In addition, we have incorporated two putative antiepileptogenic drugs, PSD95BP and 1400W, to give an insight into how such agents might ameliorate the epileptogenesis. The test drugs were administered at appropriate time-points after induction of status epilepticus (SE) and animals were euthanized at 7 days, their hippocampi removed, and subjected to LC-MS/MS analysis. A total of 2,579 proteins were identified; their normalized abundance was compared between treatment groups using ANOVA, with correction for multiple testing by false discovery rate. Significantly altered proteins were subjected to gene ontology analysis to look for enrichment of specific biological processes. KA-induced SE was most robustly associated with an increase in proteins involved in neuroinflammation, oxidative stress, cell-cell interactions and synaptic plasticity. Treatment with PSD95BP (Tat-NR2B9c) or an iNOS inhibitor, 1400W modulated several of these proteins. Our observations require validation in a larger-scale investigation, with candidate proteins explored in more detail. Nevertheless, this study has identified several mechanisms by which epilepsy might be developed and several targets for novel drug development.

2019-05-23 | PXD010986 | Pride

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