Transcriptional Response of Adult Mouse Brain to Hypoxia
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE19709 | GEO | 2011/12/30
SECONDARY ACCESSION(S): PRJNA121897
REPOSITORIES: GEO
Similar Datasets
Project description:Since normal brain function depends upon continuous oxygen delivery and short periods of hypoxia can precondition against subsequent ischemia, this study examined the effects of brief hypoxia on the whole genome transcriptional response in adult mouse brain. Genomic expression profiling was perfromed for individual brain regions of the adult mice following the entire time course of hypoxia preconditioning. Adult C57BL/6 male mice were exposed to systemic preconditioning hypoxia (8% O2 ) for 3 hr and allowed to recover in normoxia for 24 hr. The mouse brains were removed and dissected into individual brain regions at multiple time points during the 3hr hypoxia and subsequent 24hr reoxygenation periods. Total RNA was purified from the human whole blood or individual mouse brain regions. Genomic scale gene expression was then measured with Affymetrix Mouse Expression 430 2.0 arrays.
2011-12-30 | E-GEOD-19709 | biostudies-arrayexpress
Project description:Ischemic tolerance can be induced by numerous preconditioning stimuli, including various Toll-like receptor (TLR) ligands. We have shown previously that systemic administration of the TLR4 ligand, lipopolysaccharide (LPS) or the TLR9 ligand, unmethylated CpG ODNs prior to transient brain ischemia in mice confers substantial protection against ischemic damage. To elucidate the molecular mechanisms of preconditioning, we compared brain and blood genomic profiles in response to preconditioning with these TLR ligands and to preconditioning via exposure to brief ischemia. The experiment is a comparison of multiple treatment groups with sampling at multiple time points. The objective is to identify differentially regulated genes associated with preconditioning. Time points are examined both following preconditioning alone and following subsequent ischemic challenge (middle cerebral artery occlusion (MCAO)). Brain ipsilateral cortex tissue and blood were collected and processed from each animal. 6 experimental conditions: (n=3-4 mice/condition) LPS treated (i.p. 0.2mg/kg) + ischemic challenge (45min MCAO) CpG treated (i.p. 0.8mg/kg) + ischemic challenge (45min MCAO) Saline treated (i.p.) + ischemic challenge (45min MCAO) brief ischemia (12 min MCAO) + ischemic challenge (45min MCAO) Sham of brief ischemia (12 min) + ischemic challenge (45min MCAO) Non-treated + ischemic challenge (45min MCAO) Time points: Pre-ischemic challenge 3hr 24hr 72hr Post-ischemic challenge 3hr 24hr Unhandled (6 mice)-BASELINE
2011-10-04 | E-GEOD-32529 | biostudies-arrayexpress
Project description:Ischemic preconditioning is the phenomenon whereby brief periods of sublethal ischemia protect against a subsequent, more prolonged, ischemic insult. In remote ischemic preconditioning (RIPC), ischemia to one organ protects other organs at a distance. We developed mouse models to ask if inhibition of EglN1, which senses oxygen and regulates the HIF transcription factor, could suffice to mediate local and remote ischemic preconditioning. We used microarrays to detail the global expression changes induced when the oxygen sensor EglN1 is genetically deleted from skeletal muscle cells. We also used microarrays to assess the transcriptome alterations that occur in mouse hearts with pharmacologic inhibition of EglN1, using the EglN inhibitor FG-4497.
2016-02-11 | GSE77789 | GEO
Project description:Ischemic tolerance can be induced by numerous preconditioning stimuli, including various Toll-like receptor (TLR) ligands. We have shown previously that systemic administration of the TLR4 ligand, lipopolysaccharide (LPS) or the TLR9 ligand, unmethylated CpG ODNs prior to transient brain ischemia in mice confers substantial protection against ischemic damage. To elucidate the molecular mechanisms of preconditioning, we compared brain and blood genomic profiles in response to preconditioning with these TLR ligands and to preconditioning via exposure to brief ischemia. The experiment is a comparison of multiple treatment groups with sampling at multiple time points. The objective is to identify differentially regulated genes associated with preconditioning. Time points are examined both following preconditioning alone and following subsequent ischemic challenge (middle cerebral artery occlusion (MCAO)). Brain ipsilateral cortex tissue and blood were collected and processed from each animal.
2011-10-05 | GSE32529 | GEO
Project description:Ischemic preconditioning is the phenomenon whereby brief periods of sublethal ischemia protect against a subsequent, more prolonged, ischemic insult. In remote ischemic preconditioning (RIPC), ischemia to one organ protects other organs at a distance. We developed mouse models to ask if inhibition of EglN1, which senses oxygen and regulates the HIF transcription factor, could suffice to mediate local and remote ischemic preconditioning. We used microarrays to detail the global expression changes induced when the oxygen sensor EglN1 is genetically deleted from skeletal muscle cells. We also used microarrays to assess the transcriptome alterations that occur in mouse hearts with pharmacologic inhibition of EglN1, using the EglN inhibitor FG-4497. We generated mice with a tamoxifen-inducible model of EglN1 loss using a floxxed EglN1 locus with skeletal muscle-specific CRE recombinase. WT mice and mice with the floxxed EglN1 locus were exposed to tamoxifen. Mouse skeletal muscle was isolated for RNA extraction and hybridization on Affymetrix microarrays. In a related experiment, mice were treated with the EglN inhibitor FG-4497, and RNA from their heart tissue was analyzed by microarray for transcriptome alterations compared to control hearts.
2016-02-11 | E-GEOD-77789 | biostudies-arrayexpress
Project description:Prolonged cellular hypoxia leads to energetic failure and death. However, sublethal hypoxia can trigger an adaptive response called hypoxic preconditioning. While prolyl-hydroxylase (PHD) enzymes and hypoxia inducible factors (HIFs) have been identified as key elements of oxygen sensing machinery, the mechanisms by which hypoxic preconditioning protects against insults remain unclear. Here, we perform serum metabolomic profiling to assess alterations induced by hypoxic preconditioning. We discover that hypoxic preconditioning increases serum kynurenine levels and enhance kynurenine biotransformation leading to preservation of NAD+ in the post-ischemic kidney. Furthermore, we show that Indoleamine 2,3-dioxygenase 1 (Ido1) deficiency abolishes the systemic increase of kynurenine and the subsequent renoprotection generated by hypoxic preconditioning. Importantly, exogenous administration of kynurenine restores the hypoxic preconditioning in the context of Ido1 deficiency. Collectively, our findings demonstrate a critical role of Ido1/kynurenine axis in mediating hypoxic preconditioning
2021-07-01 | ST001865 | MetabolomicsWorkbench
Project description:Adult Cardiac hypoxia as a crucial pathogenesis factor can induce detrimental effects on cardiac injury and dysfunction. The global transcriptome and translatome reflecting the cellular response to hypoxia have not yet been extensively studied in myocardium. In this study, adult rats were subjected to acute normobaric hypoxia at 10% oxygen with 10 min (mild hypoxia) and 30 min (severe hypoxia). Rat H9C2 cardiomyocytes were treated with the culture condition (1% O2, 94% N2, and 5% CO2) for mild hypoxia (8 hr) and severe hypoxia(24 hr). We then conducted RNA-seq and Ribo-seq in non-infarcted left ventricular myocardial tissues and H9C2 cells exposed to different periods of hypoxia stress in vivo and in vitro.
2020-10-23 | E-MTAB-9541 | biostudies-arrayexpress
Project description:Goal was to determine differences in response to hypoxa-ischemia in the mouse brain at development stages representative of human preterm or term neonates, and to detect putative interference with spontaneous development from 2 to 15 days post-natal. Hypoxia-ischemia was realized in 5-day old and 10 day-old mice by unilateral permanent carotid ligature followed by 40 min oxygen restriction (8%). Ipsilateral hemisphere were collected at 3h, 6h 12h or 24h after hypoxia and pools of sex-equilibrated 4-6 brains were used for total RNA extraction at each time point. Co-hybridization of ishemic mRNA (labelled Cy5) and control tissues (labelled Cy3) were performed on Agilent (design 026655) micro-arrays in three independent experiments. In order to evaluate hypoxia ischemia interference during development, we evaluated spontaneous expression at P5 and P10 (Cy3) and extented the observations in a separate set of tissues extracted at P2 and P15.
2020-11-13 | GSE144456 | GEO
Project description:Age dependent effects of hypoxia-ischemia in neonatal mice brain
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Project description:Here we investigated the protein composition of the main pulmonary artery (MPA), distal pulmonary arteries (DPA) distal whole lung (DWL) of early stage hypoxia (using a neonatal bovine calf model) and late stage hypoxia (using adult steers with hypoxia-induced PH) using high resolution mass spectrometry. Compartment-resolved analysis allowed for quantitative measurements of proteins from cellular, soluble ECM and insoluble ECM fractions
2022-10-06 | MSV000090482 | MassIVE