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Global miRNA transcriptomic profiling of permanent focal ischemia in an in vivo rat model

ABSTRACT: Focal ischemia is triggered by the sudden significant reduction of blood supply to the brain, as a result of either the rupture or occlusion by thrombus/embolism of a blood vessel in the brain. Permanent focal ischemia occurred when blood supply to a specific part of the brain is impeded without reperfusion. Despite major steps achieved in the elucidation of the patho-physiology of cerebral ischemia, the available therapeutic avenues for acute ischemic stroke remain scarce. Cell cycle re-activation has been revealed as a novel signaling pathway during permanent focal ischemia. As such, non-specific aurora kinase inhibitor ZM447439, has been injected intracranial-ventricularly 30min post-ischemia induction to determine its efficacy in reduction of neuronal damage in terms of infarct volume.

ORGANISM(S): Mus musculus Rattus norvegicus Homo sapiens

PROVIDER: GSE25556 | GEO | 2013/12/31

SECONDARY ACCESSION(S): PRJNA142647

REPOSITORIES: GEO

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Global transcriptomic profiling of permanent focal ischemia in an in vivo rat model

2013-12-31 | GSE23651 | GEO

Global transcriptomic profiling of permanent focal ischemia in an in vivo rat model

Project description:Focal ischemia is triggered by the sudden significant reduction of blood supply to the brain, as a result of either the rupture or occlusion by thrombus/embolism of a blood vessel in the brain. Permanent focal ischemia occurred when blood supply to a specific part of the brain is impeded without reperfusion. Despite major steps achieved in the elucidation of the patho-physiology of cerebral ischemia, the available therapeutic avenues for acute ischemic stroke remain scarce. Cell cycle re-activation has been revealed as a novel signaling pathway during permanent focal ischemia. As such, non-specific aurora kinase inhibitor ZM447439, has been injected intracranial-ventricularly30min post-ischemia induction to determine its efficacy in reduction of neuronal damage in terms of infarct volume. Microarray analysis was performed on Illumina Rat Ref12V1 beadchips. Right cortex RNA samples were collected at two time-points (8h and 24h ) respectively for all three experimental conditions: Sham (n=4), vehicle (i.e. ischemic injury with i.c.v. injection 80% DMSO; n=4) and treatment (injury plusi.c.v.injection of 30mM ZM447439 in 80% DMSO; n=4).

2013-12-31 | E-GEOD-23651 | biostudies-arrayexpress

Global miRNA transcriptomic profiling of permanent focal ischemia in an in vivo rat model

Project description:Focal ischemia is triggered by the sudden significant reduction of blood supply to the brain, as a result of either the rupture or occlusion by thrombus/embolism of a blood vessel in the brain. Permanent focal ischemia occurred when blood supply to a specific part of the brain is impeded without reperfusion. Despite major steps achieved in the elucidation of the patho-physiology of cerebral ischemia, the available therapeutic avenues for acute ischemic stroke remain scarce. Cell cycle re-activation has been revealed as a novel signaling pathway during permanent focal ischemia. As such, non-specific aurora kinase inhibitor ZM447439, has been injected intracranial-ventricularly 30min post-ischemia induction to determine its efficacy in reduction of neuronal damage in terms of infarct volume. miRNA microarray analysis was performed on Exiqon 5th generation - hsa, mmu & rno (Product no: 208300-A) to compliment our existing gene expression microarray data [GSE23651]. Arrays were run as dual colour (Hy3: Sample, and Hy5: Common sample reference pool). Right cortex RNA samples were collected at two time-points (8h and 24h )respectively for all three experimental conditions: Sham (n=4), vehicle (i.e. ischemic injury with i.c.v. injection 80% DMSO; n=4) and treatment (injury plus i.c.v.injection of 30mM ZM447439 in 80% DMSO; n=4). Supplementary file: Project_Summary_Report.txt The percentages listed in the top row are present-call rates, i.e. number of identified miRNAs compared to number of miRNAs on array.

2013-12-31 | E-GEOD-25556 | biostudies-arrayexpress

Transcription profiling of mouse forebrain with induced middle cerebral artery occlusion (MCAO) to study permanent focal cerebral ischemia

Project description:profiling gene transcription in a mouse model of permanent focal cerebral ischemia that was induced by middle cerebral artery occlusion (MCAO)

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Common transcriptomic coding gene signature in the brain and the blood after focal brain ischemia in monkey as a tool to study neuroprotection

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Single cell expression profiling of murine subventricular zone in adult brain three days after focal celebral ischemia

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lncRNA expression signatures for stroke mice

Project description:To identify the overall impact of permanent ischemia injury on lncRNAs, we profile diﬀerentially expressed lncRNAs using microarray analysis in mouse brains subjected to permenant focal ischemia via electrocoagulation. At 24h after dMCAO injury, the animals were executed for microarray analysis of lncRNA expression.

2022-10-10 | GSE160030 | GEO

Single cell expression profiling of NG2 cell lineage from adult mice cortex three days after focal cerebral ischemia

Project description:Ischemic stroke is a serious medical condition that leads to neurological symptoms such as loss of motor and cognitive function. Focal cerebral ischemia (FCI) occurs due to interruption of blood supply to the site of injury, leading to the death of brain cells. Cells carrying Neural-glial antigen 2 (NG2) include glial cells serving primarily as olidogendrocyte precursors and a portion of pericytes. NG2 glia proliferate rapidly after ischemia and migrate to the site of injury, participate with astrocytes in glial scar formation, and contribute to the regeneration of the brain tissue. The ability of NG2 glia to differentiate into a different cell type than oligodendrocytes has been described but is still controversial. We therefore isolated NG2 cells and their derivatives labeled with tdTomato red fluorescent protein from the cortex of Rosa26-tdTomato/Cspg4-CreERT2 mice three days after middle cerebral artery occlusion (MCAO). Sham-operated animals were used as healthy controls (CTRL). We aimed to identify NG2 cell types and their derivatives in the cortex of healthy and ischemic mice and determine their incidence as well as characteristic gene expression.

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Transcriptomic changes of mouse monocytes and macrophages after ischemic stroke

Project description:Blood monocytes/macrophages infiltrate the brain after ischemic stroke and critically influence brain injury and regeneration. We investigated stroke-induced transcriptomic changes of monocytes/macrophages by RNA sequencing profiling, using a mouse model of permanent focal cerebral ischemia. Compared to non-ischemic conditions, brain ischemia induced only moderate genomic changes in blood monocytes, but triggered robust genomic reprogramming in monocytes/macrophages invading the brain. Surprisingly, functional enrichment analysis of the transcriptome of brain macrophages revealed significant overrepresentation of biological processes linked to neurovascular remodeling, such as angiogenesis and axonal regeneration, as early as 5 days after stroke, suggesting a previously underappreciated role for macrophages in initiating post-stroke brain repair. Upstream Regulator analysis predicted peroxisome proliferator-activated receptor gamma (PPARγ) as a master regulator driving the transcriptional reprogramming in post-stroke brain macrophages. Importantly, myeloid cell-specific PPARγ knockout (mKO) mice demonstrated lower post-stroke angiogenesis and neurogenesis than wild-type mice, which correlated significantly with the exacerbation of post-stroke neurological deficits in mKO mice. Collectively, our findings reveal a novel repair-enhancing transcriptome in brain macrophages during post-stroke neurovascular remodeling. As a master switch controlling genomic reprogramming, PPARγ is a rational therapeutic target for promoting and maintaining beneficial macrophage functions, facilitating neurorestoration, and improving long-term functional recovery after ischemic stroke.

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