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In vitro ischemia triggers a transcriptional response to down-regulate synaptic proteins in hippocampal neurons.

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE54037 | GEO | 2014/06/16

SECONDARY ACCESSION(S): PRJNA234394

REPOSITORIES: GEO

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In vitro ischemia triggers a transcriptional response to down-regulate synaptic proteins in hippocampal neurons.

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

Global transcriptomic profiling of oxygen-glucose deprivation (OGD)-mediated neuronal injury

Project description:Oxygen-glucose deprivation (OGD) is a cellular phenomenon consistently observed upon occurrence of ischemic stroke which eventually results in neuronal death. Neuronal cell death after ischemia takes place via two distinct processes, necrosis and apoptosis. Apoptosis, programmed cell death, is denoted by chromatin condensation, nuclear blebbing, cellular shrinkage, and DNA fragmentation. Unlike apoptosis, cellular swelling and lysis is suggestive of necrosis. However, these two processes are related not only to the severity but also to the duration of ischemia. Microarray analysis was carried out using 20 Illumina mouse Ref8V1.1 genechip arrays. The assignment of the arrays was as follows: Controls (n=5); exposure to OGD for 10min, 5h, 8h, 15h and 24 h (n=3 respectively).

2013-12-31 | E-GEOD-23158 | biostudies-arrayexpress

Genetic Screen Identified Prmt5 as a Neuroprotection Target against Cerebral Ischemia [RNA-seq]

Project description:Epigenetic regulators present novel opportunities for both ischemic stroke research and therapeutic interventions. While previous work has implicated that they may provide neuroprotection by potentially influencing coordinated sets of genes and pathways, most of them remains largely uncharacterized in ischemic conditions. In this study, we used the oxygen-glucose deprivation (OGD) model in the immortalized mouse hippocampal neuronal cell line HT-22 and carried out an RNAi screen on epigenetic regulators. We identified Prmt5 as a novel negative regulator of neuronal cell survival after OGD, which presented a phenotype of translocation from the cytosol to the nucleus upon oxygen and energy depletion both in vitro and in vivo. Prmt5 bound to the chromatin and a large number of promoter regions to repress downstream gene expression. Silencing Prmt5 significantly dampened the OGD-induced changes for a large-scale of genes, and gene ontology analysis showed that Prmt5-target genes were highly enriched for Hedgehog signaling. Encouraged by the above observation, we treated mice with middle cerebral artery occlusion (MCAO) with the Prmt5 inhibitor EPZ015666 and found that Prmt5 inhibition sustain protection against neuronal death in vivo. Together, our findings revealed a novel epigenetic mechanism of Prmt5 in cerebral ischemia and uncovered a potential target for neuroprotection.

2024-02-10 | GSE248392 | GEO

Genetic Screen Identified Prmt5 as a Neuroprotection Target against Cerebral Ischemia [ChIP-seq]

2024-02-10 | GSE248390 | GEO

Global transcriptomic profiling of oxygen-glucose deprivation (OGD)-mediated neuronal injury

2013-12-31 | GSE23158 | GEO

Global gene profiling of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-induced neuronal death

Project description:AMPA receptors are involved not only in neuronal plasticity but also in excitotoxicity, mediated largely by the influx of Ca2+ (Choi et al., 1988). Their implication has been highlighted in animal models of ischemia and epilepsy. Studies of ischemic rodent models featured that prior to cell death, hippocampal CA1 pyramidal cells exhibit an increased AMPA receptor-mediated Ca2+ influx and decreased GluR2 and GluR3 mRNA and protein levels (Gorter et al., 1997; Heuerteaux et al., 1995). A total of 15 RNA samples were analyzed. Cultured murine primary cortical neurons were treated with 300uM AMPA over a time-course of 5h, 15h and 24h (n=3) in addition to the vehicle control (n=6).

2013-12-31 | E-GEOD-22993 | biostudies-arrayexpress

miRNA profiling of control and ischemic samples in vitro and in vivo

Project description:miRNA microarray profiling of primary cortical neurons exposed to 4h oxygen and glucose deprivation (OGD) in vitro. RNA samples collected at 8h post-OGD terminaion. miRNAs were also profiled in mice exposed to 3- vessel occlusion model of stroke. RNA samples collected from contralateral (control) and ipsilateral (infarct) sides of the brain following 24h of reperfusion. Comparison of control and ischemic samples across 3 biological replicates for both in vitro and in vivo samples. In vitro cultures consisted of primary cortical neurons derived from E17 rat Wistar embryos. In vivo samples were obtained from C57bl/6 mice exposed to three-vessel occlusion.

2013-11-21 | E-GEOD-51586 | biostudies-arrayexpress

Time resolved ribosome profiling study of oxygen and glucose deprivation of rat pheochromocytoma cells

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

miRNA profiling of control and ischemic samples in vitro and in vivo

2013-11-21 | GSE51586 | GEO

An electrophysiological and proteomic analysis of the effects of the superoxide dismutase mimetic, MnTMPyP, on synaptic signalling post ischemia in isolated rat hippocampal slices.

Project description:Metabolic stress and the increased production of reactive oxygen species (ROS) are two main contributors to neuronal damage and synaptic plasticity in acute ischemic stroke (AIS). The superoxide scavenger MnTMPyP has been previously reported to have a neuroprotective effect in organotypic hippocampal slices and to modulate synaptic transmission after in vitro hypoxia and oxygen glucose deprivation (OGD). However, the mechanisms involved in the effect of this scavenger remain elusive. In this study we evaluated the concentration dependent effect of MnTMPyP on synaptic transmission during ischemia and post-ischemic synaptic potentiation. We also investigated the complex molecular changes supporting cellular adaptation to metabolic stress and how these are modulated by MnTMPyP. Electrophysiological data showed that MnTMPyP causes a concentration dependent decrease in baseline synaptic transmission and impairment of synaptic potentiation. Proteomic analysis performed on MnTMPyP treated tissue indicated an impairment in vesicular trafficking mechanisms including alteration of Secretory Carrier Membrane Protein 3 (SCAMP3) and RAB proteins and downregulation of mitochondrial-mediated apoptosis. Alterations of vesicular trafficking may lead to reduced probability of neurotransmitter release and AMPA receptor activity, resulting in the observed modulatory effect of MnTMPyP. In ischemia and glucose deprivation, protein enrichment analysis highlighted impairments in cell proliferation and differentiation, such as TGFβ1 and CDKN1B signalling, in addition to downregulation of actin signalling, cell stress and mitochondrial-mediated apoptosis. Taken together our results indicate modulation of neuronal sensitivity to the ischemic insult, and a complex role for MnTMPyP on synaptic transmission and plasticity and provide molecular insights into the mechanisms mediating the effects of MnTMPyP during ischemia

2023-05-10 | PXD040890 | Pride

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