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Expression data from Astro-D2KO mice experiencing a Status Epilepticus (SE)

ABSTRACT: Status Epilepticus (SE) is an abnormally prolonged seizure that results from either a failure of mechanisms that terminate seizures or from initiating mechanisms that inherently lead to prolonged seizures. Here we report an unbiased analysis of the hippocampal transcriptome of mice with targeted disruption of Dio2 in the astrocytes (Astro-D2KO mouse) undergoing 3 h SE.

ORGANISM(S): Mus musculus

PROVIDER: GSE114887 | GEO | 2018/05/25

REPOSITORIES: GEO

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Expression data from Astro-D2KO mice experiencing a Status Epilepticus (SE)

Project description:Expression data from Astro-D2KO mice experiencing a Status Epilepticus (SE)

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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).

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miRNA transcription profiling in Status Epilepticus Induced Epileptogenic Process

Project description:miRNA array comparing the transcription profile of control rats and rats after intra-hippocampal pilocarpine-induced Status Epilepticus (PILO-SE).

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MicroRNA profiling of rat hippocampus after status epilepticus induced by amygdala stimulation

Project description:MicroRNAs (miRNAs) are small and endogenously expressed non-coding RNAs that negatively regulate the expression of protein-coding genes at the translational level. Emerging evidence suggests that miRNAs play critical roles in central nervous system under physiological and pathological conditions. However, their expression and functions in status epilepticus (SE) have not been well characterized thus far. Here, we characterized miRNA expression profile in rat hippocampus at 24 hours following SE induced by amygdala stimulation.

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PRM validation of phosphoproteomic and proteomic analysis of early epileptogenesis in mice at 4 and 24 h post-status epilepticus

Project description:The phosphorylation-based signalling and protein changes occurring in the early phases after a pathophysiological insult, like status epilepticus (SE), have not been detailed. In a companion project, the hippocampi of mice treated with pilocarpine and diazepam were examined by tandem mass tag (TMT11plex) mass spectrometry at 4 and 24 h post-status epilepticus (PXD038241). In the accompanying article, the results implicated posttranscriptional regulatory proteins as early targets of increased phosphorylation. Also, the major targets of decreased phosphorylation at 4 h and 24 h were a subset of post synaptic density scaffold proteins, ion channels and neurotransmitter receptors. Here, the earlier work is repeated on protein and phosphorylation site targets representative of the important SE-dependent changes using parallel reaction monitoring (PRM), supporting the main findings.

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Genetic deletion of microRNA-22 blunts the inflammatory transcriptional response to status epilepticus and exacerbates epilepsy in mice

Project description:Mice lacking miR-22 displayed normal behavior and brain structure and developed similar status epilepticus after intraamygdala kainic acid compared to wildtype animals. Subsequent continuous EEG monitoring revealed an accelerated and exacerbated epileptogenesis whereby spontaneous seizures began sooner, occurred more frequently and were of longer duration in miR-22-deficient mice. RNA sequencing analysis of the hippocampus of mice during the period of epileptogenesis revealed a widespread suppression of inflammatory signalling in the hippocampus of miR-22-deficient mice. Taken together, these findings indicate a role for miR-22 in establishing early inflammatory responses to status epilepticus. Inflammatory signalling may serve anti-epileptogenic functions and cautions the timing of anti-inflammatory treatments for the treatment of status epilepticus.

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MicroRNA profiling of rat hippocampus after status epilepticus induced by amygdala stimulation

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microRNAs profiling in hippocampal cells of Self-Sustaining Status Epilepticus (SSSE) mouse model

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2014-01-01 | GSE51842 | GEO

P2X7 receptor-dependent microRNA expression profile in the brain following status epilepticus in mice

Project description:We explored the microRNA expression profile in mice lacking the P2X7 receptor before and after seizures. Genome-wide microRNA profiling was performed using hippocampi from wild-type and P2X7 knock-out mice following status epilepticus induced by intraamygdala kainic acid. This revealed that genetic deletion of the P2X7 receptor results in distinct patterns of microRNA expression. Specifically, we found that in vehicle-injected control mice the lack of P2X7 resulted in the up-regulation of 50 microRNAs and down-regulation of 35 microRNAs. Post-status epilepticus, P2X7 deficiency let to the up-regulation of 44 microRNAs while 13 microRNAs were down-regulated. Moreover, there was only limited overlap between identified P2X7-dependent microRNAs between control conditions and post-status epilepticus, suggesting P2X7 regulating the expression of different microRNAs during normal physiology and pathology. Bioinformatics analysis found that genes targeted via P2X7-dependent microRNAs were particularly overrepresented within pathways involved in intracellular signalling, inflammation and cell death, processes repeatedly linked to P2X7. Moreover, whereas genes involved in signalling pathways and inflammation were common among up-and down-regulated P2X7-dependent miRNAs during physiological and pathological conditions, genes associated with cell death seemed to be restricted to up-regulated miRNAs during both physiological conditions and post-status epilepticus. Taken together, our results demonstrate that P2X7 impacts on the expression profile of microRNAs in the brain, thereby possibly contributing to both the maintenance of normal cellular homeostasis and pathological processes.

2020-06-25 | GSE153204 | GEO

Profiling status epilepticus-induced changes in hippocampal RNA expression using high-throughput RNA sequencing

Project description:Status epilepticus (SE) is a life-threatening condition that can give rise to a number of neurological disorders, including learning deficits, depression, and epilepsy. Many of the effects of SE appear to be mediated by alterations in gene expression. To gain deeper insight into how SE affects the transcriptome, we employed the pilocarpine SE model in mice and Illumina-based high-throughput sequencing to characterize alterations in gene expression from the induction of SE, to the development of spontaneous seizure activity. While some genes were upregulated over the entire course of the pathological progression, each of the three sequenced time points (12-hour, 10-days and 6-weeks post-SE) had a largely unique transcriptional profile. Hence, genes that regulate synaptic physiology and transcription were most prominently altered at 12-hours post-SE; at 10-days post-SE, marked changes in metabolic and homeostatic gene expression were detected; at 6-weeks, substantial changes in the expression of cell excitability and morphogenesis genes were detected. At the level of cell signaling, KEGG analysis revealed dynamic changes within the MAPK pathways, as well as in CREB-associated gene expression. Notably, the inducible expression of several noncoding transcripts was also detected. These findings offer potential new insights into the cellular events that shape SE-evoked pathology.

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