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MicroRNAs profiling in hippocampal cells of mouse with Pilocarpine-induced Status Epilepticus (SE)

ABSTRACT: SE was induced in mice (NMRI) chemically by a single dose of Pilocarpine (300mg/kg;i.p.). RNA was extracted from the hippocampi of treated and wild-type mice at 24 h and 28 d after induction. microRNA expressions were measured via microarray technology using Exiqon's miCURY™ LNA Arrays.

ORGANISM(S): Merkel cell polyomavirus Rattus norvegicus Mus musculus Human gammaherpesvirus 8 JC polyomavirus Betapolyomavirus macacae Homo sapiens Murid gammaherpesvirus 4 Human immunodeficiency virus 1 Human betaherpesvirus 5 Human alphaherpesvirus 2 Human alphaherpesvirus 1 Betapolyomavirus hominis human gammaherpesvirus 4 Mus musculus cytomegalovirus 2

PROVIDER: GSE51841 | GEO | 2014/01/01

SECONDARY ACCESSION(S): PRJNA225587

REPOSITORIES: GEO

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microRNAs profiling in hippocampal cells of mouse with Pilocarpine-induced Status Epilepticus (SE)

Project description:SE was induced in mice (NMRI) chemically by a single dose of Pilocarpine (300mg/kg;i.p.). RNA was extracted from the hippocampi of treated and wild-type mice at 24 h and 28 d after induction. microRNA expressions were measured via microarray technology using Exiqon's miCURY™ LNA Arrays. 4 conditions, Pilocarpine treated mice at 24 h and 28 d, and the control wild-type at the same types, each of 8 replicates.

2014-01-01 | E-GEOD-51841 | biostudies-arrayexpress

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.

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Quantitative analysis of hippocampal transcriptomes of naïve and post-status epilepticus (SE) mouse with or without levetiracetam (LEV).

Project description:LEV is known to be involved in neuroprotection via anti-angiogenesis and anti-inflammatory activities against blood-brain barrier dysfunction in the acute phase of epileptogenesis after SE, but the mechanism remains unclear. The purpose of this study is to comprehensively examine the gene expression in hippocampus of LEV-treated and untreated pilocarpine induced (PILO-) SE mouse in order to understand the whole process of early epileptogenesis.

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

2014-01-01 | E-GEOD-51842 | biostudies-arrayexpress

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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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, have not been detailed. To this end, the hippocampi of mice treated with pilocarpine and diazepam were examined by mass spectrometry at 4 and 24 h post-status epilepticus at vast depth using the tandem mass tag 11-plex system. 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. Many proteins targeted by dephosphorylation at 4 h also had decreased protein abundance at 24 h, indicating a phosphatase-mediated weakening of synapses.

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microRNAs profiling in hippocampal cells of mouse with Sound-induced Seizure

Project description:After an electrically induced seizure, mice (NMRI) received electrical stimulation (current intensity 44 mA, 0.2 ms monopolar pulses at 6 Hz frequency for 3 s). RNA was extracted from the hippocampi at 0, 3, 6, 24 and 72 h after the seizure. microRNA expressions were measured via microarray technology using Exiqon's miCURY™ LNA Arrays.

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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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Rosiglitazone polarizes microglia and protects against pilocarpine-induced status epilepticus.

Project description:AimsActivated microglia have been found in the forebrains and hippocampi of temporal lobe epilepsy (TLE) patients and status epileptic (SE) animal models. The peroxisome proliferator-activated receptor γ (PPAR γ) agonist rosiglitazone has been shown to prevent microglial activation. However, its role in pilocarpine-induced status epilepticus remains unknown. We aimed to examine the effect of the PPAR γ agonist rosiglitazone in protecting against pilocarpine-induced status epileptic resulting from over-activation and to explore phenotypic changes in microglia as the underlying mechanism.MethodsMale C57BL/6 mice were assigned to three groups: the control group, pilocarpine-induced (SE) group, and rosiglitazone-treated (SE+Rosi) group. Status epileptic mice were administered 300 mg/kg pilocarpine via intraperitoneal injection. SE+Rosi mice were administered rosiglitazone (0.1 mg/kg, i.p.) after SE. Flow cytometry, immunofluorescence staining, and quantitative real-time PCR were used to examine the activation of and phenotypic changes in microglia in the brain and to evaluate neuroinflammation.ResultsWe found that the expression of proinflammatory CD86 and iNOS was increased and that the expression of antiinflammatory CD206 and Arg-1 was decreased in the brains of pilocarpine-induced SE mice compared to control mice. The mRNA levels of proinflammatory and antiinflammatory cytokines were not significantly changed in the brain. Rosiglitazone treatment significantly inhibited the proinflammatory polarization of microglia and rescued neuron loss in the temporal lobe and hippocampi of the brain after SE.ConclusionRosiglitazone reverses microglial polarization in the brains of SE mice and also affords neuroprotection against pilocarpine-induced status epilepticus without inducing significant changes in brain inflammation.

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Differential expression of pancreatic cancer PANC1 cells treated with pilocarpine

Project description:Human Panc1 cells were treated with 1mM Pilocarpine and the differential expression measured by RNASeq

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