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MicroRNA-124 and -137 cooperativity controls caspase-3 activity through BCL2L13 in hippocampal neural stem cells. [miRNA expression]

ABSTRACT: Temporal lobe epilepsy (TLE) can develop from alterations in hippocampal structure and circuit characteristics, and can be modeled in mice by administration of kainic acid (KA). Adult neurogenesis in the dentate gyrus (DG) contributes to hippocampal functions and has been reported to contribute to the development of TLE. Some of the phenotypical changes include neural stem and precursor cells (NPSC) apoptosis, shortly after their birth, before they produce hippocampal neurons. Here we explored these early phenotypical changes in the DG 3 days after systemic KA administration to mice. Our specific aim was to understand the molecular mechanisms underlying altered apoptosis levels in NSPC following KA-induced status epilepticus (KA-SE). Accordingly, we chose a multi-omics experimental setup and analyzed DG tissue samples using proteomics, transcriptomics and microRNA profiling techniques. We here present a description of how these date were obtained and provide them to others for further analysis and validation. This may help to further identify and characterize molecular mechanisms involved in the alterations induced shortly after KA-SE in the mouse DG. Total RNA obtained from dentate gyrus 72h after mice were subjected to repeated low dose kainic acid induced status epilepticus or saline i.p. injections

ORGANISM(S): Mus musculus

SUBMITTER: Marijn Schouten

PROVIDER: E-GEOD-79131 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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MicroRNA-124 and -137 cooperativity controls caspase-3 activity through BCL2L13 in hippocampal neural stem cells. [RNA expression]

Project description:Temporal lobe epilepsy (TLE) can develop from alterations in hippocampal structure and circuit characteristics, and can be modeled in mice by administration of kainic acid (KA). Adult neurogenesis in the dentate gyrus (DG) contributes to hippocampal functions and has been reported to contribute to the development of TLE. Some of the phenotypical changes include neural stem and precursor cells (NPSC) apoptosis, shortly after their birth, before they produce hippocampal neurons. Here we explored these early phenotypical changes in the DG 3 days after systemic KA administration to mice. Our specific aim was to understand the molecular mechanisms underlying altered apoptosis levels in NSPC following KA-induced status epilepticus (KA-SE). Accordingly, we chose a multi-omics experimental setup and analyzed DG tissue samples using proteomics, transcriptomics and microRNA profiling techniques. We here present a description of how these date were obtained and provide them to others for further analysis and validation. This may help to further identify and characterize molecular mechanisms involved in the alterations induced shortly after KA-SE in the mouse DG. Total RNA obtained from dentate gyrus 72h after mice were subjected to repeated low dose kainic acid induced status epilepticus or saline i.p. injections

2016-03-12 | E-GEOD-79129 | biostudies-arrayexpress

MicroRNA-124 and -137 cooperativity controls caspase-3 activity through BCL2L13 in hippocampal neural stem cells. [miRNA expression]

2016-03-12 | GSE79131 | GEO

MicroRNA-124 and -137 cooperativity controls caspase-3 activity through BCL2L13 in hippocampal neural stem cells. [RNA expression]

2016-03-12 | GSE79129 | GEO

iTRAQ-based proteomic analysis of dentate gyrus in temporal lobe epilepsy with hippocampal sclerosis

Project description:Temporal lobe epilepsy (TLE) is the most frequent type of focal epilepsy in adults, typically resistant to pharmacological treatment and mostly present with cognitive impairment and psychiatric comorbidities. The most common neuropathological hallmark in TLE patients is hippocampal sclerosis(HS). However, the underlying molecular mechanisms involved remain poorly characterized. Dentate gyrus(DG), one specific hippocampal subarea, structural and functional changes imply a key involvement of the DG in the development of TLE. In this study, isobaric tags for relative and absolute quantitation (iTRAQ) -based quantitative proteomic technique was performed to analysis of hippocampal DG obtained from patients with TLE-HS compared to control samples obtained from the autopsy. Our proteomic data identified 5583 proteins, of which 82 proteins were up-regulated and 90 proteins were down-regulated. Bioinformatics analysis indicated that differential expressed proteins enriched in “synaptic vesicle”, “mitochondrion”, “cell-cell adhesion”, “regulation of synaptic plasticity”, “ATP binding” and “Oxidative phosphorylation”. Protein-protein interaction network analysis found a pivotal module of 10 proteins that relate to “Oxidative phosphorylation”. This study is the first to investigate proteomic alterations in DG region of TLE-HS patients, and pave the way to better understanding of epileptogenesis mechanisms and future therapeutic intervention.

2021-01-18 | PXD023048 | Pride

Expression data in the mouse brain following the glucocorticoid receptor overexpression in the forebrain (GRov) during different periods in development

Project description:The glucocorticoid receptor overexpression in early life is sufficient to alter gene expression patterns for the rest of the animal's life. Hippocampal dentate gyrus (DG) are more responsive than the nucleus accumbens (NAcc) following the glucocorticoid receptor overexpression in the forebrain. Laser capture microdissection was performed. Microdissected areas from the dentate gyrus or nucleus accumbens were collected from serial sections for each animal.

2012-03-15 | E-GEOD-30187 | biostudies-arrayexpress

MicroRNA-124 and -137 cooperativity controls caspase-3 activity through BCL2L13 in hippocampal neural stem cells.

Project description:Adult neurogenesis continuously contributes new neurons to hippocampal circuits and the programmed death of a subset of immature cells provides a primary mechanism controlling this contribution. Epileptic seizures induce strong structural changes in the hippocampus, including the induction of adult neurogenesis, changes in gene expression and mitochondrial dysfunction, which may all contribute to epileptogenesis. However, a possible interplay between this factors remains largely unexplored. Here, we investigated gene expression changes in the hippocampal dentate gyrus shortly after prolonged seizures induced by kainic acid, focusing on mitochondrial functions. Using comparative proteomics, we identified networks of proteins differentially expressed shortly after seizure induction, including members of the BCL2 family and other mitochondrial proteins. Within these networks, we report for the first time that the atypical BCL2 protein BCL2L13 controls caspase-3 activity and cytochrome C release in neural stem/progenitor cells. This work has been published in Sci Rep. 2015 Jul 24;5:12448. doi: 10.1038/srep12448.

2016-03-14 | PXD003744 | Pride

Estrogen protects neurotransmission transcriptome during status epilepticus

Project description:Epilepsy in women is often accompanied by hormonal disturbances including irregular cycles and premature onset of menopause. Decline in estrogen levels results in increased risk for neurodegenerative diseases, with strong participation of chronic inflammation. We have shown that estradiol (EB) has neuroprotective effects against seizure-induced damage in the sensitive hilar region of hippocampal dentate gyrus associated with neuropeptide Y (NPY) upregulation. Here, we quantify the alterations caused by kainic acid-induced status epilepticus in the glutamatergic, GABAergic, dopaminergic, cholinergic and serotonergic synapse transcriptomes of dentate gyrus of ovariectomized female rats and the recovery effects of the EB replacement. Our data indicate that the EB replacement reduces the number of significantly regulated genes in seizured ovariectomized female rats by about 45%. The new measure Pathway Restoration Efficiency (PRE) indicates the dopaminergic synapse to be the most protected (65%) and the GABAergic synapse the least protected (37%) by the EB replacement.

2017-12-06 | GSE107725 | GEO

Genome-wide analysis of kainic acid-induced gene expression in dentate gyrus from CTR and SRF knockout mice.

Project description:To identify genes regulated by SRF in response to increased neuronal activity whole-genome expression profiling (Illumina Mouse WG-6 microarrays) of kainic acid-induced genes were performed. We found that loss of SRF in DG leads to specific deficits in activity-induced gene expression. Identified genes functions are associated with synapse plasticity, epilepsy, outgrowth of neurites, behavior and MAPK signaling pathway. The microarray experiment was performed to identify SRF-dependent activity-induced genes, using brain-specific, inducible SRF gene knockout mice. Conditional mutants of Srf were obtained by crossing mice in which Srf gene was flanked by loxP sites (Srf f/f) with an CaMKCreERT2 line to ablate its expression exclusively in excitatory forebrain neurons. Knockouts (KO = Srf f/f;CaMKCreERT2) and control littermates (CTR = Srf f/f) were used in the experiments. To enable time-specific induction of SRF deletion, adult mice, were injected with tamoxifen. Global gene expression induced by kainic acid (KA, 35-50 mg/kg) was analyzed. At 6 hours after seizures induction (seizures severity 5; according to modified Racine scale) or saline injection, CTR and KO animals were sacrificed and dentate gyrus was microdissected and used for RNA isolation. In order to identify SRF-regulated genes, we used Illumina MouseWG-6 v2.0 Expression BeadChips.

2015-02-02 | E-GEOD-60772 | biostudies-arrayexpress

Expression data in the mouse brain following the glucocorticoid receptor overexpression in the forebrain (GRov) during different periods in development

2012-03-15 | GSE30187 | GEO

Identification of differentially expressed genes in the hippocampus in the intraamygdala kainic acid mouse model of status epilepticus.

Project description:The aim of this work was to identify mRNA expression changes in the ipsilateral hippocampus in the intraamygdala kainic acid (KA) mouse model of status epilepticus. In this model, status epilepticus (prolonged damaging seizures) are triggered by an intraamygdala KA injection. All mice develop epilepsy after a short latency period of 3-5 days. For our experiments, 10-week old mice with a C57BL/6 background were either injected with intraamygdala KA (n = 18) or vehicle (PBS, n = 18). Mice were sacrificed 8 hours following status epilepticus (acute pathology) or 14 days post-status epilepticus (timepoint at which all mice suffer from chronic epilepsy) and ipsilateral hippocampi were quickly dissected and pooled into 3 groups (n = 3 per pooled sample).

2021-09-09 | GSE122228 | GEO

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