E-GEOD-56267
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA242801
DISEASE(S): Normal,Cortical Ischemic Stroke
PROVIDER: E-GEOD-56267 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-56267-analysis-methods.tsv | Tabular | |||
| E-GEOD-56267-analytics.tsv | Tabular | |||
| E-GEOD-56267-analytics.tsv.undecorated | Tabular | |||
| E-GEOD-56267-analytics.tsv.undecorated.unrounded | Tabular | |||
| E-GEOD-56267-analytics.tsv.unrounded | Tabular |
Items per page: 5 1 - 5 of 23 |
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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
Project description:It has been unclear whether ischemic stroke induces neurogenesis or neuronal DNA-rearrangements in the human neocortex. We show here that neither is the case, using immunohistochemistry, transcriptome-, genome- and ploidy-analyses, and determination of nuclear bomb test-derived 14C-concentration in neuronal DNA. A large proportion of cortical neurons display DNA-fragmentation and DNA-repair short time after stroke, whereas neurons at chronic stages after stroke show DNA-integrity, demonstrating the relevance of an intact genome for survival. Analyze of potential fusion transcripts in 13 samples, seven cortical ischemic stroke tissue and six control cortex, by deep sequencing using Illumina HiSeq 2000
2014-03-28 | E-GEOD-56267 | biostudies-arrayexpress
Project description:The human cerebral cortex depends for its normal development and size on a precisely controlled balance between self-renewal and differentiation of diverse neural progenitor cells. Specialized progenitors that are common in humans, but virtually absent in rodents, called â??outer radial gliaâ?? (ORG), have been suggested to be crucial to the evolutionary expansion of the human cortex. We combined cell type-specific sorting with transcriptome-wide RNA-sequencing to identify genes enriched in human ORG, including targets of the transcription factor Neurogenin, and previously uncharacterized, evolutionarily dynamic, long noncoding RNAs. Single-cell transcriptional profiling of human, ferret, and mouse progenitors showed that more human RGC co-express proneural Neurogenin targets than in ferret or mouse, suggesting greater self-renewal of neuronal lineage-committed progenitors in humans. Finally, we show that activating the Neurogenin pathway in ferret RGC promotes delamination and outward migration. Thus, we find that the abundance of human ORG is paralleled by increased transcriptional heterogeneity of cortical progenitors. Three biological replicates of human late mid-fetal cortex (18 to 19 weeks of gestation) were dissociated and immunolabeled. Apical and outer radial glial cells were purified by FACS and compared to an immunonegative population, predominantly neurons.
2015-02-24 | E-GEOD-66217 | biostudies-arrayexpress
Project description:We report the identification of enhancer domains in sham and stroke mouse cerebral cortices by high-throughput profiling of H3K27Ac chromatin modification. A total of 35.4, 28.8 and 29.6 million reads were generated from chromatin immunoprecipitated DNA from sham, stroke and pooled input samples. This resulted in 55,571 peaks in sham and 56,110 peaks in stroke samples representing 50408 and 51,292 active regions, respectively. These active regions represent putative enhancer domains.
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Project description:The layered structure of the cerebral cortex is formed through a complicated sequence of highly controlled stages. During this process, the perturbations of neuronal migration and cell division can result in a rare disorder called cortical heterotopia. Heterotopia patients can have recurrent epileptic seizures, developmental delays, and mild intellectual disabilities. Studying heterotopia has been challenging because human mutations linked to the disease often do not result in heterotopia formation in mouse models. EML1 is a microtubule-binding protein, and it stands out as the first heterotopia-associated gene where mutations lead to heterotopia formation in both humans and mice. In this study, we conducted a comparative proteomic analysis of the Eml1 cKO heterotopic mice cortices and neuronal progenitor primary cells during cerebral cortex development. We performed label-free and dimethyl labeling-based quantitative proteomic approaches, and microtubule pelleting assays to understand how Eml1 depletion disrupts protein networks in cortical tissue and neuronal progenitor primary cells during cerebral cortex development.
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Project description:Recent advances in high-throughput transcriptomics have revealed extensive gene expression changes during cerebral ischemia. However, the changes in 3D chromatin architecture and long-range chromatin looping between genes and distal regulatory elements that drive these gene expression changes remain virtually unexplored. In this study, we mapped the landscape of altered 3D chromatin looping the in the ischemic cortex and evaluated its contributions to post-stroke transcriptional changes. We used genome-wide chromatin conformation capture (Hi-C) to profile changes in the 3D chromatin architecture in the cerebral cortex of adult mice following a 1 h middle cerebral artery occlusion and 6 h of reperfusion, or sham surgery. We identified a total of 15,592 loops in the stroke group with a mean enrichment core of 6.108, and these included 1973 promoter-promoter contacts, 7857 enhancer-enhancer contacts, and 5762 enhancer-promoter contacts. In the sham group, there were 14,779 chromatin loops with a mean enrichment score of 5.473, including 1714 promoter-promoter contacts, 8597 enhancer-enhancer contacts, and 4468 enhancer-promoter contacts. Together, our study represents the first genome-wide evaluation of 3D chromatin looping following stroke.
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Project description:Acute ischemic stroke (AIS) is a leading cause of disability and mortality worldwide. By high-throughput sequencing of infarct and ischemic penumbra tissue from middle cerebral artery embolization (MCAO) mice, we identified the CircRNA expression was dramatically and selectively regulated in the penumbra tissues.
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Project description:Evolution of the mammalian brain encompassed a remarkable increase in size of cerebral cortex, including tangential and radial expansion, but the mechanisms underlying these key parameters are still largely unknown. Here, we identified the novel DNA associated protein TRNP1 as a regulator of cerebral cortical expansion in both these dimensions. Gain and loss of function experiments in the mouse cerebral cortex in vivo demonstrate that high Trnp1 levels promote neural stem cell self-renewal and tangential expansion, while lower levels promote radial expansion resulting in a potent increase in the generation of intermediate progenitors and outer radial glial cells resulting in folding of the otherwise smooth murine cerebral cortex. Remarkably, TRNP1 expression levels exhibit regional differences also in the cerebral cortex of human fetuses anticipating radial or tangential expansion respectively. Thus, the dynamic regulation of TRNP1 is critical to regulate tangential and radial expansion of the cerebral cortex in mammals. We performed gene expression microarray analysis on embryonic mouse cerebral cortex derived from Trnp1 knockdown and control animals.
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Project description:The human cerebral cortex depends for its normal development and size on a precisely controlled balance between self-renewal and differentiation of diverse neural progenitor cells. Specialized progenitors that are common in humans, but virtually absent in rodents, called ‘outer radial glia’ (ORG), have been suggested to be crucial to the evolutionary expansion of the human cortex. We combined cell type-specific sorting with transcriptome-wide RNA-sequencing to identify genes enriched in human ORG, including targets of the transcription factor Neurogenin, and previously uncharacterized, evolutionarily dynamic, long noncoding RNAs. Single-cell transcriptional profiling of human, ferret, and mouse progenitors showed that more human RGC co-express proneural Neurogenin targets than in ferret or mouse, suggesting greater self-renewal of neuronal lineage-committed progenitors in humans. Finally, we show that activating the Neurogenin pathway in ferret RGC promotes delamination and outward migration. Thus, we find that the abundance of human ORG is paralleled by increased transcriptional heterogeneity of cortical progenitors.
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