RNA sequencing of ipsilateral cortex after transient focal ischemia in mice
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ABSTRACT:
PROVIDER: PRJNA544489 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9114790_1.fastq.gz | Fastqsanger.gz | |||
| SRR9114790_2.fastq.gz | Fastqsanger.gz | |||
| SRR9114800_1.fastq.gz | Fastqsanger.gz | |||
| SRR9114800_2.fastq.gz | Fastqsanger.gz | |||
| SRR9114791_1.fastq.gz | Fastqsanger.gz |
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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
Project description:Effect of transient focal ischemia on circular RNAs
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Project description:Voluntary running exercise after focal cerebral ischemia promotes functional recovery and prevents the ischemia-induced dendritic spine loss in the peri-infarct motor cortex layer 5. Neuronal morphology is affected by the perineuronal environmental change. Glia exert crucial roles in the formation of perineuronal environment, and exercise-induced changes of glial phenotype are expected. Here, we demonstrated that voluntary running exercise increased the population of newborn astrocytes in the acute phase after cerebral ischemia at late phase. Transcriptome analysis detected 10 upregulated genes and 70 downregulated genes by exercise in the ipsilateral cortex astrocytes. Gene cluster downregulated by exercise were significantly associated with neuronal morphology. The expression of Lipocalin 2, a factor of decreasing dendritic spines, tended to be decreased in the postischemic astrocytes by exercise. Our results suggest that exercise modifies the phenotype of postischemic astrocytes, which relate to the exercise-induced amelioration of postischemic dendritic spine loss.
2022-08-08 | GSE210674 | GEO
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
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.
2023-09-21 | E-MTAB-11967 | biostudies-arrayexpress
Project description:To investigate the potential involvement of circRNA in ischemic pathophysiology, we performed a circRNA microarray in an established transient middle cerebral artery occlusion (MCAO) mouse model of stroke. We evaluated the expression of 1797 circRNAs in adult mice brain after tMCAO. In our study, 5 of the 1178 circRNAs analyzed in the circRNA array were up-regulated significantly, ≥1.5-fold, in ischemic cortex at 12 hours of reperfusion after MCAO compared with their levels in sham group.
2020-09-25 | GSE115697 | GEO
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
Project description:Estrogen reduces brain injury after experimental cerebral ischemia in part through a genomic mechanism of action. Using DNA microarrays, we analyzed the genomic response of the brain to estradiol, and we identified a transcript, cocaine- and amphetamine-regulated transcript (CART), that is highly induced in the cerebral cortex by estradiol under ischemic conditions. Using in vitro and in vivo models of neural injury, we confirmed and characterized CART mRNA and protein up-regulation by estradiol in surviving neurons, and we demonstrated that i.v. administration of a rat CART peptide is protective against ischemic brain injury in vivo. We further demonstrated binding of cAMP response element (CRE)-binding protein to a CART promoter CRE site in ischemic brain and rapid activation by CART of ERK in primary cultured cortical neurons. The findings suggest that CART is an important player in estrogen-mediated neuroprotection and a potential therapeutic agent for stroke and other neurodegenerative diseases. Experiment Overall Design: affy platform; replicate samples; two treated samples, two placebo. Experiment Overall Design: MIAME compliance: All samples were run in commercial arrays from Affymetrix, using Rat Genome U34A GeneChip arrays as described in the Affymetrix web site. The sample information is described below. Likewise, the Affymetrix protocol is detailed and referenced above. These descriptions include all information currently considered under the MIAME supportive guidelines, with which the JHMI Microarray Core Facility abides in all its procedures. Experiment Overall Design: Methodology. Expression profiling using DNA microarrays (One round amplification): Experiment Overall Design: Experimental Design and Sample Information. Transient focal cerebral ischemia was induced in ovariectomized female rats with and without replacement with 17beta-estradiol by intraluminal middle cerebral artery occlusion (MCAO), as described in the manuscript. At 6 and 24 hours after 2-hour MCAO, total RNA was prepared from the ischemic and contralateral cerebral cortex and striatum between coronal levels 2 and 3 mm relative to Bregma, which represent the core of MCA territory. RNA samples from 3 animals were combined into one pooled sample and hybridized to Affymetrix RG-U34A GeneChip, as described below. Each microarray experiment was performed in duplicate using two independent pooled samples per group (6 animals per group at each time point, 2 pooled samples for each brain region per time point). Experiment Overall Design: Microarray Hybridization Protocol. Total RNA was isolated using the RNeasy Mini Kit (QIAGEN). RNA from control and experimental tissue are processed using the RNA amplification protocol described by Affymetrix (Affymetrix Expression Manual). Briefly, 5 micrograms of total RNA were used to synthesize first strand cDNA using oligonucleotide probes with 24 oligo-dT plus T7 promoter as primer (Proligo LLC, Boulder, Colorado) and the SuperScript Choice System (Invitrogen, Carlsbad, California). Following the double stranded cDNA synthesis, the product was purified by phenol-chloroform extraction, and biotinilated anti-sense cRNA was generated through in vitro transcription using the BioArray RNA High Yield Transcript Labeling kit (ENZO Life Sciences Inc., Farmingdale, New York). 15 ug of the biotinilated cRNA were fragmented at 94 C for 35 min (100mM Tris-acetate, pH 8.2, 500mM KOAc, 150mM MgOAC), and 10ug of total fragmented cRNA were hybridized to the Affymetrix U34A GeneChip arrays for 16hr at 45 C with constant rotation (60 rpm). Affymetrix Fluidics Station 450 was then used to wash and stain the Chips, removing the non-hybridized target and incubating with a streptavidin-phycoerythrin conjugate to stain the biotinilated cRNA. The staining was then amplified using goat IgG as blocking reagent and biotinilated anti-streptavidin antibody (goat), followed by a second staining step with a streptavidin-phycoerythrin conjugate. Experiment Overall Design: Quality Control. To ascertain the quality control of the total RNA from the samples, we used the Agilent Bioanalyzer, Lab on a Chip technology, and confirmed the rRNA ratios and clean run patterns of the samples. Likewise, this technology is used to confirm the quality of the RNA in the form of cRNA and fragmented cRNA. To assess the QC of the hybridization, GeneChip image, and comparison between chips, we confirmed the following parameters: scaling factor values within comparable range; low background values (50-95); high percentage of present calls (between 30 and 55%); consistent 3â/5â ratios of GAPDH as representation of housekeeping genes, and presence or absence of Bio B and C as internal spike controls.
2008-06-13 | E-GEOD-5315 | biostudies-arrayexpress
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.
2013-12-31 | GSE23651 | GEO
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.
2013-12-31 | GSE25556 | GEO