Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA131563 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Ischemia lead to neuronal injury. Dexmedetomidine and astrocytes are likely to protect neuronal cells against ischemia-induced injury. We used microarrays to examine the gene expression variation in astrocytes activated by oxygen-glucose deprivation and reoxygenation stress and identified distinct classes of genes up- and down-regulated by dexmedetomidine pretreatment.
2021-02-05 | GSE166193 | GEO
Project description:Brain microvascular endothelial cell (BMEC) injury can affect neuronal survival by modulating immune responses through the microenvironment. We used microarrays to detail the miRNAs expression in the exosomes from normal and oxygen glucose deprivation (OGD)-cultured BMECs.
2023-03-08 | GSE224961 | GEO
Project description:Global transcriptomic profiling of lactacystin-mediated neuronal death
| PRJNA128621 | ENA
Project description:Global transcriptomic profiling of nitric oxide-mediated neuronal death
| PRJNA128937 | ENA
Project description:The present study has used whole-rat genome microarray expression profiling to identify genes whose expression is significantly altered in hippocampal neuronal cultures submitted to oxygen and glucose deprivation (OGD), an established in vitro model for cerebral global ischemia that is suitable for investigations at the molecular level. To do so, total RNA was extracted from hippocampal neuronal cultures at an early (7h) and delayed (24h) time point after OGD, as well as from control neurons. Analysis of gene ontology showed that OGD followed by 7h or 24h of recovery induces changes in the expression levels of genes related with inflammation, response to oxidative stress, metabolism, apoptosis, synaptic proteins and ion channels and, importantly, genes that show different expression levels are mainly specific to one of the two time points of recovery analyzed. The expression levels of several genes were confirmed by qPCR and were in good agreement with the microarray data, showing that the combined use of the OGD model and the microarray technology can be a useful tool for the study molecular mechanisms contributing to the neuronal demise after transient global ischemia. Ischemia induced gene expression in primary hippocampal neuronal rat cultures was measured at 7 and 24 hours after exposure to Oxygen and Glucose deprivation (OGD). Three independent experiments were performed at each time (7 or 24 hours) as independent biological replicates.
2014-06-16 | E-GEOD-54037 | biostudies-arrayexpress
Project description:Gene expression profiling was performed to identify Siah2-dependent changes in cells subjected to ER stress, hypoxia, and combined glucose/oxygen deprivation. To establish the magnitude of the Siah2 effect on the ER stress response, we have compared gene expression profiles of WT and Siah1a-/-::Siah2-/- mouse embryo fibroblasts (MEFs) that were subjected to glycosylation inhibitor tunicamycin (TM), thapsigargin (TG), glucose deprivation, or glucose/oxygen deprivation. Overall, this analysis confirmed changes associated with ER stress that had not previously been associated with Siah2 signaling, substantiating Siah2 as a key coordinator of ER stress through the ATF4 and sXbp1 pathways. WT and Siah1a/Siah2 KO MEF cells were treated with TM or TG for 6 h, or subjected for 12 h to oxygen deprivation, glucose deprivation or a combination of oxygen and glucose deprivation, in duplicate.
2014-04-01 | E-GEOD-39244 | biostudies-arrayexpress
Project description:Neurogenesis is a pro-survival process that comprises of dendritic and axonal growth, synaptogenesis, synaptic and neuronal pruning. These complex processes are determined by temporal gene expression during development, which is in turn tightly regulated by long non-coding RNAs and microRNAs. In this study, we investigated the processes implicated in the maturation of primary neuronal cultures based on RNA expression profiling. Correlation between neuron specific gene ontologies of mRNA and non-coding RNAs identified direct regulation of axonogenesis and dendritogenesis. Temporally regulated mRNA and their associated long non-coding RNAs were significantly overrepresented in proliferation and differentiation associated signalling, cell adhesion molecules and neurotrophin signalling pathways during neuronal maturation. Long non-coding RNAs associated with Axin2, Cntn1, Ncam1, Negr1, Ntrk2, Nrxn1 and Sh2b3 displayed an inverse expression profile to their mRNA whereas long non-coding RNA -mRNA pairs for Kit, Prkcb and Ralgds displayed similar expression profiles. These genes were also predicted targets of the altered miRNAs, miR-124, -128, -129-5p, -203, -218, -290-5p, -326, -329, -377 and -495. These microRNAs particularly regulate the cell adhesion molecules, Cntn1, Ncam1, Negr1 and Nrxn1 that determine axonogenesis and dendritogenesis, supporting the observed co-regulation of these biological processes by non-coding RNAs. Verification of expression of these long non-coding RNA-mRNA pairs in an in vitro model of ischemic-reperfusion injury showed an inverse expression profile, thus confirming their role(s) in maintenance of the neuronal structure and function. This neuronal transcriptome (mRNAs, lncRNAs, miRNAs) is in turn orchestrated by C/EBPM-NM-1/M-NM-2 transcription factors and CTCF, thereby governing intricate control of neuronal development. mRNA and long non-coding RNA expression profiling of maturing primary cortical neurons from E15 mouse embryos and neurons subjected to oxygen-glucose deprivation. Maturing neurons were harvested on Days 2, 4, 6 and 8. Neurons on Day 6 were subjected to oxygen-glucose deprivation for different time periods and 24 hours reperfusion before being harvested.
2014-10-24 | E-GEOD-44833 | biostudies-arrayexpress
Project description:Oxygen and glucose metabolism plays a pivotal role in many (patho)physiological conditions. In particular, oxygen and glucose deprivation (OGD) occurs during ischemia and stroke, resulting in extensive tissue injury and cell death. We applied time-resolved ribosome profiling technique to assess early events at the level of gene expression in rat pheochromocytoma PC12 cells during short-term OGD. Most substantial alterations in transcripts levels and their translation were seen to occur in the first 20 minutes of OGD. The rapid adaptation of translation apparatus to OGD is global and involves altered elongation and initiation rates. We also observed salient and reproducible alterations in ribosome densities of individual mRNAs such as increased translation of particular upstream Open Reading Frames (uORFs); induced site-specific arrests of the ribosomes and synthesis of extended protein isoforms. Ribosome profiling (with mRNA-seq sequencing) was carried out at 0,20,40 and 60 minutes of OGD. Two biological replicates were used.
2015-04-10 | E-GEOD-60752 | biostudies-arrayexpress
Project description:Nitric oxide (NO) is implicated in the pathogenesis of various neuropathologies characterised by oxidative stress. NO has been reported to be involved in the exacerbation of oxidative stress by various mechanisms, including protein modification, genotoxic damage and elevated production of reactive oxygen species resulting in deregulation and disruption of cellular homeostasis. Although multiple roles for NO has been reported in neuronal death signaling, existent data fail to provide a holistic description of how nitrergic pathobiology elicits neuronal injury. Here we provide a comprehensive description of mechanisms contributing to NO-induced neuronal injury by global transcriptomic profiling. Microarray analysis was carried out using 14 GeneChip Mouse Genome 430 2.0 array (Affymetrix, Santa Clara, CA). The assignment of the arrays (GeneChip) was as follows: vehicle-treated control (n=5); NOC-18-treatment for 8, 15 and 24 hour (n=3 for each time-point).
2013-01-23 | E-GEOD-22087 | biostudies-arrayexpress
Project description:Nitric oxide (NO) is implicated in the pathogenesis of various neuropathologies characterised by oxidative stress. NO has been reported to be involved in the exacerbation of oxidative stress by various mechanisms, including protein modification, genotoxic damage and elevated production of reactive oxygen species resulting in deregulation and disruption of cellular homeostasis. Although multiple roles for NO has been reported in neuronal death signaling, existent data fail to provide a holistic description of how nitrergic pathobiology elicits neuronal injury. Here we provide a comprehensive description of mechanisms contributing to NO-induced neuronal injury by global transcriptomic profiling.
2013-01-23 | GSE22087 | GEO