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Global transcriptomic profiling of ischemic/reperfusion injury in an in vivo wild-type mouse model.

ABSTRACT: Ischemic stroke triggers severe focal hypoperfusion accompanied with deprivation of oxygen and glucose to the cerebral tissue, together with loss of ATP, depolorization of neurons, elevated extracellular potassium concentration, and subsequently leads to excitotoxicity as well as increased oxidative stress promoting microvascular injury, blood-brain-barrier deregulation, post-ischemic inflammation and eventually the consequential neurological deficit. Although reperfusion of ischemic brain tissue is critical for restoring normal function, it can paradoxically result in secondary damage, called ischemia/reperfusion (I/R) injury.

ORGANISM(S): Mus musculus

PROVIDER: GSE23160 | GEO | 2011/01/10

SECONDARY ACCESSION(S): PRJNA133269

REPOSITORIES: GEO

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Global transcriptomic profiling of ischemic/reperfusion injury in an in vivo wild-type mouse model.

Project description:Ischemic stroke triggers severe focal hypoperfusion accompanied with deprivation of oxygen and glucose to the cerebral tissue, together with loss of ATP, depolorization of neurons, elevated extracellular potassium concentration, and subsequently leads to excitotoxicity as well as increased oxidative stress promoting microvascular injury, blood-brain-barrier deregulation, post-ischemic inflammation and eventually the consequential neurological deficit. Although reperfusion of ischemic brain tissue is critical for restoring normal function, it can paradoxically result in secondary damage, called ischemia/reperfusion (I/R) injury. Microarray analysis was performed on the right striatum and cortex (corresponded to infarct area) of post-I/R injured brain tissues of wild-type (WT-MCAO) using Illumina mouse Ref8 V2 genechips. Suture-induced middle cerebral artery occlusion was induced for 2h followed by reperfusion, with tissue extraction taking place 2h, 8h and 24h post-reperfusion (n=4 respectively). Sham controls were included in this study too (n=4 respectively).

2011-01-10 | E-GEOD-23160 | biostudies-arrayexpress

small RNA-Seq of rat kidney in a model of ischemic preconditioning/ischemia-reperfusion injury

Project description:Ischemic preconditioning is effective in limiting subsequent ischemic acute kidney injury in experimental models. microRNAs are an important class of post-transcriptional regulator and show promise as biomarkers of kidney injury. An evaluation was performed of the time- and dose-dependent effects of ischemic preconditioning in a rat model of functional (bilateral) ischemia-reperfusion injury. A short, repetitive sequence of ischemic preconditioning resulted in optimal protection from subsequent ischemia-reperfusion injury. A detailed characterization of microRNA expression in ischemic preconditioning/ischemia-reperfusion injury was performed by small RNA-Seq.

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Exiqon miRCURY microRNA array of rat kidney in a model of ischemic preconditioning/ischemia-reperfusion injury

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Global transcriptomic profiling of ischemic/reperfusion injury in an in vivo mouse model.

Project description:This SuperSeries is composed of the following subset Series: GSE23160: Global transcriptomic profiling of ischemic/reperfusion injury in an in vivo wild-type mouse model. GSE23162: Global transcriptomic profiling of ischemic/reperfusion injury in an in vivo Gpx1 -/- transgenic mouse model. Refer to individual Series

2011-01-10 | E-GEOD-23163 | biostudies-arrayexpress

Vascular Permeability and Apoptosis are Separable Processes in Retinal Ischemia-Reperfusion Injury

Project description:Effects of Ischemic Preconditioning, Bevacizumab and Etanercept Ischemia and reperfusion injury provides an acute model of ischemic retinopathy that includes neurodegeneration and VEGF-dependent vascular permeability and is amenable to rapid drug testing. The distinct effects of ischemic preconditioning and bevacizumab demonstrate that the apoptotic and vascular responses to ischemia may be separated and that VEGF expression is not neuroprotective following ischemic-reperfusion. Using transient ischemia followed by reperfusion (IR) to model ischemic retinal disease, this study compares the effects of ischemic preconditioning (IPC) and therapies targeting vascular endothelial growth factor (VEGF) and tumor necrosis factor α (TNFα) on retinal apoptosis, vascular permeability and mRNA biomarker expression. Only the Ischemic Preconditioning (not Bevacizumab and Etanercept treated samples) were hybridized to arrays. Study contains 6 replicates of control and 6 IP treated retinal samples.

2010-05-31 | E-GEOD-20521 | biostudies-arrayexpress

Vascular Permeability and Apoptosis are Separable Processes in Retinal Ischemia-Reperfusion Injury

2010-06-01 | GSE20521 | GEO

Transcriptional changes during hepatic ischemia-reperfusion in the rat

Project description:Ischemia-reperfusion (IR) injury, a ubiquitous consequence of liver transplantation, is a cause of early graft rejection and increased morbidity. At present, there are no effective strategies to reduce hepatic IR injury. Molecular mechanisms that promote cell survival under these circumstances are largely undefined. We examined changes in global gene expression at early reperfusion times to identify potential IR-mediated protective responses. Using a rat model of 30 minutes of 70% warm ischemia followed by reperfusion, RNA for microarray analysis was extracted from the non-ischemic and the ischemic-reperfused lobes at four reperfusion times: 0 (no reperfusion), 0.5, 2, and 6 hours. Differentially expressed genes and pathway analyses were used to identify IR-induced events. The transcriptome of the reperfused lobes was unique and discrete at each reperfusion time, showing no evidence of sustained changes of the gene expression alterations seen at 30 minutes of reperfusion. At all reperfusion times, a significant portion of gene expression changes in the reperfused lobes were present in the non-ischemic lobes. However, the earliest reperfusion time, 30 minutes, showed a marked increase in the expression of a set of immediate-early genes (c-Fos, c-Jun, Atf3, Egr1) that was exclusive to the reperfused lobe. Similarities of gene expression changes in the reperfused and the non-ischemic lobes at each time suggest that hemodynamics and/or circulating factors are potent stimuli in an IR model. However, early reperfusion events appear to reflect a cell-autonomous response that may be protective, thereby representing potential targets to ameliorate IR injury.

2019-12-16 | GSE117915 | GEO

Proteomic analysis of focal cerebral ischemia/reperfusion injury in rats

Project description:Stroke is a leading cause of mortality and long-term disability and ischemic stroke accounts for 87% of all strokes. Though timely recanalization of the occluded vessel is essential in the treatment of ischemic stroke, it is well known to cause ischemia-reperfusion (I/R) injury which result in neuronal cell death, brain tissue loss and severe neurological deficits. In this work, we employed a global proteomic approach to examine the changes of cerebral cortex proteins in rats undergoing acute and long-term I/R injury. In vivo middle cerebral artery occlusion (MCAO) model of focal cerebral I/R injury in rats was established. The animals were divided into three model groups with 2 h-MCAO followed with different reperfusion time, 1 day, 7 days and 14 days, respectively. For each model group a sham group was correspondingly set. Each group included four animals. For proteomic analysis, cerebral cortex proteins were extracted and analyzed by SDS-PAGE, whole-lane slicing, in-gel digestion and label-free quantitative LC-MS/MS. A total of 5621 proteins were identified and their quantities between the surgery and corresponding sham groups and across the three reperfusion time points were compared for mechanism investigation. This dataset includes all the raw files of the 840 LC-MS runs (6 groups x 4 animals x 35 gel squares/sample), as well as their identification and quantitation results at the levels of peptide fragments, peptides and proteins, respectively.

2019-07-03 | PXD012151 | Pride

The analysis of differential gene expression after remote ischemic preconditioning of renal ischemia reperfusion injury

Project description:To investigate the mechanism by which ischemic preconditioning (IPC) produces tissue tolerance to renal ischemia reperfusion injury in a pig model

2016-09-02 | GSE72646 | GEO

Gene expression data from remote ischemic postconditioning in rat model of ischemia reperfusion injury

Project description:Restoration of blood flow is the definitive therapy to salvage myocardium following ischemic injury. However, sudden restoration of blood flow to the ischemic myocardium causes ischemia reperfusion injury (IRI). Here, the cardioprotective effect of remote ischemic postconditioning (RPostC) was investigated, based on our in vitro rat model of myocardial IRI. Three groups, including Sham, IRI, and IRI+ RPostC, were utilized for the analysis of Affymetrix Rat Gene 2.0 ST chip.

2019-05-15 | GSE122020 | GEO

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