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Profiling brain cortex from tMCAO rat stroke model

ABSTRACT: This program addresses the gene signature associated with brain (cortex) in the tMCAO rat model for stroke.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE38037 | GEO | 2013/03/22

SECONDARY ACCESSION(S): PRJNA167174

REPOSITORIES: GEO

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Profiling brain cortex from tMCAO rat stroke model

Project description:This program addresses the gene signature associated with brain (cortex) in the tMCAO rat model for stroke. The tMCAO stroke model profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in brain cortex of the Sprague Dawley rats following middle cerebral artery occlusion compared to the sham-operated controls.

2013-03-22 | E-GEOD-38037 | biostudies-arrayexpress

The role of a mammalian network in regulating ischemic stroke outcome II

Project description:To detect mRNAs in ischemic stroke animals we dissected contralateral (CL) and peri-ischemic (PI) cortex of transient middle cerebral artery occlusion (tMCAo) mice wild-type and ciRS-7 KO We performed differentially expression analysis of RNA-seq of wild-type and ciRS-7 KO tMCAo ischemic mice

2023-01-31 | GSE213177 | GEO

Rattus norvegicus

Project description:Profiling brain cortex from tMCAO rat stroke model

| PRJNA167174 | ENA

RNA sequencing of ipsilateral cortex after transient focal ischemia in mice

Project description:We report the application of Illumina paired-end RNA-seq approach for transcriptome of brain tissue in mice. By removing sequence-dependent bias and amplification noise using UMI-tools. The mapped reads of each sample were assembled using StringTie. After the final transcriptome was generated, StringTie and edgeR was used to estimate the expression levels of all transcripts. By obtaining a total of million paired-end reads of sequence from cerebral cortex tissue, we generated transcriptome profiles of mouse ischemic cortex in sham, 24 h after focal ischemia, 28 d after focal ischemia, with or without neuron-specific knockdown of TIPARP, respectively. We found 2017 differentially expressed genes (DEGs) between Sham+AAV-SYN-shRNA-Con and tMCAO+AAV-SYN-shRNA-Con group, and 516 DEGs between tMCAO+AAV-SYN-shRNA-Con and tMCAO+AAV-SYN-shRNA-TIPARP group at 24 h after stroke. In addition, we found 487 DEGs between Sham+AAV-SYN-shRNA-Con and tMCAO+AAV-SYN-shRNA-Con group, and 192 DEGs between tMCAO+AAV-SYN-shRNA-Con and tMCAO+AAV-SYN-shRNA-TIPARP group at 28 d after stroke. This study provides a detailed analysis of the underlying mechanisms of neuron-specific knockdown of TIPARP in neuronal injury and long-term effect, with biologic replicates, generated by RNA-seq technology.

2022-05-22 | GSE131712 | GEO

Rattus norvegicus brain tissue samples: Sham-operated vs. Remote limb postconditioning (PostC) and Sham-operated vs. transient middle cerebral artery occlusion (tMCAO)

Project description:Transcriptional profiling of miRNAs from rat brain tissues comparing controls (Sham) with ischemic rats (tMCAO) and neuroprotected rats (RLIP) Internal normalization: ischemic core vs. periischemic and ANOVA comparison across three experimental conditions: Sham, tMCAO and RLIP

2021-09-30 | GSE184975 | GEO

C57BL/6J tMCAO brain scRNAseq data

Project description:Single Cell RNA sequencing data from C57BL/6J mouse brain hemisphere after 24hours and 48hours after tMCAO surgery.

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Proteomic alterations in microglia with ischemic stroke and effect of LPS treatment

Project description:Ischemic stroke is a common acute CNS disorder leading to nearly half a million deaths per year in Europe. The high mortality is primarily owed to the limited treatment options of restoring blood flow in a narrow time window of several hours. Furthermore, inflammatory processes in the days and weeks after ischemic stroke contribute to tissue loss and neurological deficits. The key cells that influence and control this inflammatory cascade are microglia, the innate immune cells of the CNS. Microglia can be influenced and activated by e.g. lipopolysaccharide (LPS),a bacterial cell membrane component. It has been previously shown, that repetitive LPS stimuli prior to infarction (termed immunological preconditioning) lead to reduced infarct volumina in mouse models of ischemic stroke. Furthermore, our laboratory has shown, that phosphoinositide-3 kinase gamma mediates microglial functions after LPS-preconditioning. Hence, the aim of this work was to characterize proteomic alterations in microglia with (I) ischemic stroke in general in the tMCAO (transient middle cerebral artery occlusion) mouse model of ischemic stroke, (II) the influence of LPS-preconditioning on microglial proteomic alterations after tMCAO and (III) the role of PI3Ky in the microglial proteomic changes after tMCAO and preconditioning. This was done by a single LPS injection 3 days before tMCAO in wildtype mice and mice with PI3Ky knockout or knockin of the kinase dead form of PI3Ky.

2024-03-22 | PXD031930 | Pride

Ndufc2 gene contributes to stroke susceptibility in the stroke-prone spontaneously hypertensive rat and it associates with juvenile ischemic stroke occurrence in humans

Project description:To investigate genetic basis of stroke susceptibility in an animal model of complex human disease, the stroke-prone spontaneously hypertensive rat (SHRSP).

2016-06-26 | E-MTAB-3688 | biostudies-arrayexpress

Stroke-induced transcriptomic alterations in mouse cerebral microvessels

Project description:To investigate the stroke-induced changes in gene expression in cerebral microvessels, we subjected mice to transient middle cerebral artery occlusion (tMCAO) or sham surgeries. 24h hours later, cerebral microvessels were harvested and RNA was isolated. We then performed gene expression profiling analysis using data obtained from RNA-seq of cerebral microvessels isolated from 8 mice (4 shams and 4 tMCAO)

2022-12-24 | GSE221379 | GEO

Deletion of LOX-1 has protective effects on ischemic brain damage in the genetic background of stroke-prone spontaneously hypertensive rat

Project description:To explore the impact of oxidized low density lipoprotein receptor 1 (Olr1 aka LOX-1) gene on stroke, we newly generate a LOX-1 deficient strain of the genetic background of stroke-prone spontaneously hypertensive rat (SHRSP). We explored circulatory miRNAs as diagnostic biomarkers for cerebral ischemic injury by microarray analysis in related rat strains.

2020-05-19 | E-MTAB-8389 | biostudies-arrayexpress

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