Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression changes in HT-22 cells with or without PGC-1α overexpression upon OGD stimulation

ABSTRACT: PGC-1α overexpression in neurons protects against chronic cerebral hypoperfusion-induced cognitive impairment in mice. To investigate the neuroprotective mechanism of PGC-1α, we employed RNA-Seq analysis on PGC-1α-overexpressed HT-22 cells, a hippocampal neuron cell line. We performed OGD experiment to mimick chronic cerebral hypoperfusion. Indeed, PGC-1α overexpression alters the gene expression profiles of HT-22 cells, suggesting that neuronal PGC-1α might play an important role after chronic cerebral hypoperfusion.

ORGANISM(S): Mus musculus

PROVIDER: GSE127788 | GEO | 2019/03/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profiles in hippocampus with or without neuronal PGC-1α overexpression

Project description:Upregulation of neuronal PGC-1α ameliorates cognitive impairment induced by chronic cerebral hypoperfusion in mice. To investigate the underlying mechanism of PGC-1α, we have employed whole mRNA microarray expression profiling as a discovery platform to identify genes with the potential to change the hippocampal function. Indeed, PGC-1α overexpression alters the gene expression profiles of hippocampus, this suggested that neuronal PGC-1α might play an important role after chronic cerebral hypoperfusion.

2019-07-16 | GSE134257 | GEO

Gene expression changes in HT-22 cells with or without PGC-1α overexpression upon OGD stimulation

Project description:Gene expression changes in HT-22 cells with or without PGC-1α overexpression upon OGD stimulation

| PRJNA525403 | ENA

RNAseq of mouse corpus callosum from WT or TRPA1-KO animals under chronic cerebral hypoperfusion

Project description:Chronic cerebral hypoperfusion is manifested in various CNS diseases accompanied by cognitive impairment, such as dementia, however the precise mechanism of chronic cerebral hypoperfusion-induced cognitive impairment remains unknown. Recently, transient receptor potential ankyrin 1 (TRPA1), activated by oxidative stress, was reported to be involved in the cerebrovascular diseases, therefore we investigated the pathophysiological role of TRPA1 in chronic cerebral hypoperfusion using a mouse bilateral common carotid artery stenosis (BCAS) model. Early cognitive impairment and white matter injury was induced by BCAS in TRPA1-knockout (TRPA1-KO) but not wild-type (WT) mice. For further investigation into the involvement of TRPA1 in chronic cerebral hypoperfusion, we conducted RNA sequence (RNAseq) in the corpus callosum from sham- and BCAS-operated WT and TRPA1-KO mice.

2023-08-08 | GSE201513 | GEO

PHD inhibition upregulates glycolytic pathway in OGD

Project description:To elucidate the mechanism of enarodustat pretreatment-induced protection against oxygen-glucose deprivation (OGD), we have we have employed whole genome microarray expression profiling as a discovery platform to identify genes upregulated by enarodustat exposure. HK2 cells were pretreated with either vehicle (DMSO) or enarodustat for 24 hours prior to OGD for 16 hours. Pathway analysis revealed upregulated glysolysis pathway.

2020-04-14 | GSE130144 | GEO

Hippocampus miRNA profiles in chronic cerebral-hypoperfusion rats

Project description:Hippocampus miRNA profiles in chronic cerebral-hypoperfusion rats

| PRJNA595889 | ENA

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

Gene expression profile at single cell level of microglia sorted from rats brain with chronic cerebral hypoperfusion

Project description:Microglia are considered as a heterogenous population in the brain tissues. We used single-cell RNA sequencing (scRNA-seq) to analyze the diversity of microglia in the rats with chronic cerebral hypoperfusion.

2024-08-26 | GSE234247 | GEO

Remodeling of Brown and White Adipose Tissue by NT-PGC-1α-Mediated Gene Regulation

Project description:The β-adrenergic receptor signaling pathway is a major component of adaptive thermogenesis in brown and white adipose tissue during cold acclimation. The β-AR activation highly induces transcriptional coactivator PGC-1α and its splice variant N-terminal (NT)-PGC-1α, promoting the transcription program of mitochondrial biogenesis and thermogenesis. In the present study, we evaluated the role of NT-PGC-1α in brown adipocyte energy metabolism by genome-wide profiling of NT-PGC-1α-responsive genes. Canonical pathway analysis revealed that a number of genes upregulated by NT-PGC-1α are highly enriched in mitochondrial pathways including fatty acid transport and β-oxidation, TCA cycle and electron transport system, thus reinforcing the crucial role of NT-PGC-1α in the enhancement of mitochondrial function. Moreover, gene expression profiling of NT-PGC-1α revealed activation of distinct metabolic pathways such as glucose, lipid and nucleotide metabolism and of signaling pathways such as RAR and PPAR-γ/RXRα activation in brown adipocytes. Together, our data strengthen our previous findings that NT-PGC-1α is a key regulator of mitochondrial oxidative metabolism and thermogenesis in brown adipocytes and further suggest that NT-PGC-1α influences a broader spectrum of thermogenic processes to meet cellular needs for adaptive thermogenesis. Two samples from two groups: NT-PGC-1α overexpression and empty vector. There are technical replicates (A and B) for each group. Two RNA samples were pooled for each group.

2015-08-07 | E-GEOD-71774 | 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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data