Altered Biogenesis and MicroRNA Content of Hippocampal Exosomes Following Experimental Status Epilepticus
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ABSTRACT:
PROVIDER: PRJNA563073 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10050215.fastq.gz | Fastqsanger.gz | |||
| SRR10050216.fastq.gz | Fastqsanger.gz | |||
| SRR10050217.fastq.gz | Fastqsanger.gz | |||
| SRR10050218.fastq.gz | Fastqsanger.gz | |||
| SRR10050219.fastq.gz | Fastqsanger.gz |
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Project description:Here, we characterised the effects of experimental status epilepticus on the expression of exosome biosynthesis components and analysed microRNA content in exosome-enriched fractions prepared from the mouse hippocampus. Status epilepticus induced by unilateral intra-amygdala kainic acid resulted in acute subfield-specific, bi-directional changes in transcripts associated with exosome biosynthesis including up-regulation of ESCRT–dependent and –independent pathways. Increased expression of exosome components including Alix were detectable in samples obtained two weeks after status epilepticus and changes occurred in both the ipsilateral and contralateral hippocampus. Small RNAseq analysis of exosome-enriched fractions prepared using two different techniques detected a rich diversity of conserved microRNAs and determined status epilepticus selectively alters microRNA contents, including upregulation of the glia-enriched miR-21a-3p. We also characterized editing sites of the exosome-enriched miRNAs and found six exosome-enriched miRNAs that were Adenosine-to-Inosine (ADAR) edited with the majority of the editing events predicted to occur within miRNA seed regions. However, the prevalence of these editing events was not altered by status epilepticus. These studies demonstrate status epilepticus alters the exosome pathway and its microRNA content, but not editing patterns.
2019-12-12 | GSE136695 | GEO
Project description:Repetitive or prolonged seizures (status epilepticus) can damage neurons within the hippocampus, trigger gliosis, and generate an enduring state of hyperexcitability. Recent studies have suggested that microvesicles including exosomes are released from brain cells following stimulation and tissue injury, conveying contents between cells including microRNAs (miRNAs). Here, we characterized the effects of experimental status epilepticus on the expression of exosome biosynthesis components and analyzed miRNA content in exosome-enriched fractions. Status epilepticus induced by unilateral intra-amygdala kainic acid in mice resulted in acute subfield-specific, bi-directional changes in hippocampal transcripts associated with exosome biosynthesis including up-regulation of endosomal sorting complexes required for transport (ESCRT)-dependent and -independent pathways. Increased expression of exosome components including Alix were detectable in samples obtained 2 weeks after status epilepticus and changes occurred in both the ipsilateral and contralateral hippocampus. RNA sequencing of exosome-enriched fractions prepared using two different techniques detected a rich diversity of conserved miRNAs and showed that status epilepticus selectively alters miRNA contents. We also characterized editing sites of the exosome-enriched miRNAs and found six exosome-enriched miRNAs that were adenosine-to-inosine (ADAR) edited with the majority of the editing events predicted to occur within miRNA seed regions. However, the prevalence of these editing events was not altered by status epilepticus. These studies demonstrate that status epilepticus alters the exosome pathway and its miRNA content, but not editing patterns. Further functional studies will be needed to determine if these changes have pathophysiological significance for epileptogenesis.
| S-EPMC6978807 | biostudies-literature
Project description:miRNA array comparing the transcription profile of control rats and rats after intra-hippocampal pilocarpine-induced Status Epilepticus (PILO-SE).
2016-04-28 | E-MTAB-4633 | biostudies-arrayexpress
Project description:Transient brain insults including status epilepticus (SE) can initiate a process termed ‘epileptogenesis’ that results in chronic temporal lobe epilepsy (TLE). As a consequence, the entire tri-synaptic circuit of the hippocampus is fundamentally impaired. A key role in epileptogenesis has been attributed to the CA1 region as the last relay station in the hippocampal circuit and as site of aberrant plasticity, e.g. mediated by acquired channelopathies. The transcriptional profiles of the distinct hippocampal neurons are highly dynamic during epileptogenesis. Here, we aimed to elucidate the early SE-elicited mRNA signature changes and the respective upstream regulatory cascades in CA1. RNA sequencing of CA1 was performed in the mouse pilocarpine-induced SE model at multiple time points ranging from 6 to 72 hours after the initial insult. Bioinformatics was used to decipher altered gene expression, signalling cascades and their corresponding cell type profiles. Robust transcriptomic changes were detected at 6h after SE and at subsequent time points during early epileptogenesis. Major differentially expressed mRNAs encoded primarily immediate early and excitability-related gene products, as well as genes encoding immune signalling factors.
2023-12-20 | GSE241219 | GEO
Project description: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.
2018-05-25 | GSE114887 | GEO
Project description:Highly dynamic inflammatory and excitability transcriptional profiles in hippocampal CA1 following status epilepticus
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Project description:Status Epilepticus (SE) is induced in mice (C57Bl/6J) through electrical stimulation (90min, 100 ms trains of 1 ms, 2 trains per 1 s, 250 μA peak current intensity). RNA was extracted from the hippocampi at 24 h and 28 d after induction. In wild-type RNA was extracted on the 22nd day. microRNA expressions were measured via microarray technology using Exiqon's miCURY™ LNA Arrays.
2014-01-01 | GSE51842 | GEO
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
Project description:Status Epilepticus (SE) is induced in mice (C57Bl/6J) through electrical stimulation (90min, 100 ms trains of 1 ms, 2 trains per 1 s, 250 μA peak current intensity). RNA was extracted from the hippocampi at 24 h and 28 d after induction. In wild-type RNA was extracted on the 22nd day. microRNA expressions were measured via microarray technology using Exiqon's miCURY™ LNA Arrays. 3 conditions, SSSE mouse model at 24 h and 28 d, and a control group, each of 8 replicates.
2014-01-01 | E-GEOD-51842 | biostudies-arrayexpress
Project description:In this study we used microarray analysis to reveal the gene expression profile of the hippocampal CA1 subregion, which was laser-capture microdissected one week after kainic acid (KA)-induced status epilepticus (SE) in postnatal day 21 (P21) rats. These rats are developmentally roughly comparable to juvenile children, and KA-induced SE leads to selective damage of hippocampal CA1 pyramidal neurons in this age group while saving neurons of the other sub-regions. We searched for alterations in the gene expression pattern during the early epileptogenetic phase, i.e. one week after SE, and compared the results with those of age-matched control rats. To detect specifically changes in the CA1 pyramidal neurons, we used the laser-capture microdissection technique that allows the precise isolation of the region of interest. The RNA of this region was isolated, amplified, and labeled, and then hybridized to Illumina RatRef-12 Expression BeadChip Arrays. The gene expression data generated from the microarray was first normalized by the guantile normalization method, and then filtered by using the empirical Bayes method, and the contrasts were created by using the Limma R/Bioconductor. Finally, the data was clustered by using the non-hierarchical K-means clustering for genes, and the pathway analysis was performed by âGene set testâ, which analyzes the statistical significance of a set of genes simultaneously ranked by p-value and generates the KEGG categories (Chipster manual). The Illumina microarray analysis with the Chipster software v1.1.0 (http://chipster.csc.fi; CSC, Espoo, Finland) generated a total of 1592 differently expressed genes in the CA1 subregion of KA-treated rats compared to control rats. Using the K-means method the genes were classified in 10 different clusters. The subsequent KEGG-test for the probe set over-representation analysis revealed the 15 significantly (p<0.05) changed KEGG-pathways in response to KA-treatment, e.g. oxidative phosphorylation (26 genes changed), and long-term potentiation (LTP; 18 genes changed). Some of the differentially expressed genes were also identified to be involved in Ca2+ homeostasis, gliosis, inflammation, and GABAergic transmission.
2010-10-25 | E-TABM-881 | biostudies-arrayexpress