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Altered Biogenesis and MicroRNA Content of Hippocampal Exosomes Following Experimental Status Epilepticus

ABSTRACT: Altered Biogenesis and MicroRNA Content of Hippocampal Exosomes Following Experimental Status Epilepticus

PROVIDER: PRJNA563073 | ENA |

REPOSITORIES: ENA

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			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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Altered Biogenesis and MicroRNA Content of Hippocampal Exosomes Following Experimental Status Epilepticus

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

Altered Biogenesis and MicroRNA Content of Hippocampal Exosomes Following Experimental Status Epilepticus.

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

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

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

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

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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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Differential DNA Methylation Patterns Define Status Epilepticus and Epileptic Tolerance

Project description:Comparison of methylation profiles in the CA3 region of the mouse hippocampus in epileptic tolerance and status epilepticus.

2012-02-09 | E-MEXP-3503 | biostudies-arrayexpress

Highly dynamic inflammatory and excitability transcriptional profiles in hippocampal CA1 following status epilepticus

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

Estrogen protects neurotransmission transcriptome during status epilepticus

Project description:Estrogen protects neurotransmission transcriptome during status epilepticus

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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).

2021-09-09 | GSE122228 | 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.

2015-08-27 | GSE72402 | GEO

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