Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Temporal study of the effect of acute systemic inflammation on the cerebral endothelial cells (CECs) and microglia in mice

ABSTRACT: Temporal study of the effect of acute systemic inflammation on the cerebral endothelial cells (CECs) and microglia in mice

PROVIDER: PRJNA649977 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12363200_1.fastq.gz	Fastqsanger.gz
	SRR12363200_2.fastq.gz	Fastqsanger.gz
	SRR12363201_1.fastq.gz	Fastqsanger.gz
	SRR12363201_2.fastq.gz	Fastqsanger.gz
	SRR12363202_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

Temporal study of the effect of acute systemic inflammation on the cerebral endothelial cells (CECs) and microglia in mice

Project description:To capture the global gene expression patterns in the CECs and microglia following acute systemic inflammation, we injected the mice with LPS and sacrificed them after 30 min, 1 hr and 2 hrs, immediately followed by the isolation of the brains and dissociation to yield single cell suspension, immunolabelling and finally flow assisted cell sorting of CECs (CD45- CD13- CD31+) and microglia (CD45 low-mid CD11b+). RNA was then isolated from the cells followed by RNA-seq.

2020-12-10 | GSE155517 | GEO

LPS-induced systemic inflammation mediates a protective effect against ischemic injury via microglia

Project description:LPS-induced systemic inflammation mediates a protective action on ischemic injury via microglia. We used RNA sequencing analysis (RNA-seq) to gain molecular insights into microglia-mediated protection of cerebral infarction.

2023-12-19 | GSE244358 | GEO

Effect of acute systemic inflammation on the Cerebral Vasculature in mice

Project description:To capture the global gene expression patterns in the cerebral vasculature following acute systemic inflammation, we injected the mice with LPS and sacrificed them after 15 min, 30 min, and 4 hrs, followed by the isolation of the cerebral vessels. RNA was isolated from the vessel lysates, followed by library preparation and RNA sequencing.

2020-12-10 | GSE155516 | GEO

Microglia regulate basal cerebral blood flow and neurovascular coupling through ectonucleotidase CD39 II

Project description:Microglia modulate cerebral blood flow and cerebrovascular reactivity, but the mechanisms remain elusive. Here we show that pharmacological or genetic method induced microglia-ablation, which causes reduction of the microglia-expressed ATP/ADP-hydrolyzing ectonucleotidase CD39, elevates the cerebral blood flow baseline, while reducing the cerebral blood flow change to whisker stimulation and intra-cisterna magna injection of ATP, but not adenosine. Microglia P2ry12 inhibition with clopidogrel increased basal cerebral blood flow and the effect was abolished in microglia specific CD39 knockout mice. P2ry12 knockout mice show reduced cerebral blood flow changes to whisker stimulation or intra-cisterna magna injection of ATP. Microglia-specific deletion of CD39 or its pharmacological inhibition reproduces the effects of microglia ablation on cerebral blood flow and attenuates whisker stimulation-induced adenosine concentration increase in contralateral barrel cortex. These results suggest that microglia-dependent adenosine production is an integral component of the brain purinergic signaling system that governs neurovascular coupling.

2024-06-01 | GSE245107 | GEO

Transcriptomic profiling of microglia from a model of Experimental Cerebral Malaria Transcriptomic profiling of microglia from a model of Experimental Cerebral Malaria

Project description:Cerebral malaria is a pathology involving inflammation in the brain. There are many immune cell types activated during this process, but there is little information on the contribution of microglia, the brain resident macrophages, to this severe complication. We have examined the responses of microglia in a model of experimental cerebral malaria (ECM), in which C57BL/6 mice are infected with Plasmodium berghei ANKA. Genome wide transcriptomic analysis of these cells revealed that thousands of transcripts were differentially expressed at two different time points during the infection. The analysis indicated that proliferation of microglia was a dominant feature before the onset of ECM, and supporting this, we observed an increase in numbers of these cells in the brain. When cerebral malaria symptoms were manifest, genes involved in immune responses and chemokine production were upregulated, which were possibly driven by Type I Interferon. Together, our data offer a unique insight into the responses of microglia in the brain during ECM.

2016-12-19 | GSE86082 | GEO

Effect of acute systemic inflammation on the Cerebral Vasculature in mice

Project description:Effect of acute systemic inflammation on the Cerebral Vasculature in mice

| PRJNA649971 | ENA

Transcriptomic analysis of mouse brain microglia on aging-associated changes in response to cerebral ischemia

Project description:Senescence-associated alterations in microglia may have profound impact on cerebral homeostasis and stroke outcomes. However, the lack of a transcriptome-wide comparison between young and aged microglia in the context of ischemia limits our understanding of aging-related mechanisms. Herein, we performed bulk RNA sequencing analysis of microglia purified from cerebral hemispheres of young adult (10-week-old) and aged (18-month-old) mice 5 days after distal middle cerebral artery occlusion or sham operation. Considerable transcriptional differences were observed between young and aged microglia in healthy brains, indicating heightened chronic inflammation in aged microglia. Following stroke, the overall transcriptional activation was more robust in young microglia than in aged microglia. Gene clusters with functional implications in immune inflammatory responses, immune cell chemotaxis, tissue remodeling, and cell-cell interactions were markedly activated in microglia of young but not aged stroke mice. These alterations in microglial gene response may contribute to aging-driven vulnerability and poorer recovery after ischemic stroke.

2020-05-31 | GSE145265 | GEO

Microglia and the immune response to a human temporal lobe seizure

Project description:Inflammatory processes and cells of the immune system including brain-resident microglia are activated in the epilepsies. We examined shape, transcriptomic profile and expression of microglial markers in tissue from the temporal lobe of epileptic patients. In the basal state, transcripts and pathways associated with the anti-inflammatory cytokine IL10, were up-regulated in the tissue from more sclerotic regions. We found that seizures also induce dynamic immune responses and change microglial phenotype. A pseudo-temporal ordering of the delay between the last seizure and tissue and analysis, based on immediate early gene expression, indicated an initial and local, innate immune response. At longer pseudo-time delays, infiltration of extra-cerebral cells, principally T-cells, contributed to the immune response. Ictal-like activity or ADP application in slices reproduced microglial activation including changes in motility and the liberation of inflammatory cytokines.

2022-03-18 | GSE94744 | GEO

Microglia contributes to remyelination in cerebral but not spinal cord ischemia

Project description:Inflammation after injury of the central nervous system (CNS) is increasingly viewed as a therapeutic target. However, comparative studies in different CNS compartments are sparse. To date only few studies based on immunohistochemical data and all referring to mechanical injury have directly compared inflammation in different CNS compartments. These studies revealed that inflammation is more pronounced in spinal cord than in brain. Therefore, it is unclear whether concepts and treatments established in the cerebral cortex can be transferred to spinal cord lesions and vice versa or whether immunological treatments must be adapted to different CNS compartments. By use of transcriptomic and flow cytometry analysis of equally sized photothrombotically induced lesions in the cerebral cortex and the spinal cord, we could document an overall comparable inflammatory reaction and repair activity in brain and spinal cord between day 1 and day 7 after ischemia. However, remyelination was increased after cerebral versus spinal cord ischemia which is in line with increased remyelination in grey matter in previous analyses and was accompanied by microglia dominated inflammation opposed to monocytes/macrophages dominated inflammation after spinal cord ischemia. Interestingly remyelination could be reduced by microglia and not hematogenous macrophage depletion. Our results show that despite different cellular composition of the postischemic infiltrate the inflammatory response in cerebral cortex and spinal cord are comparable between day 1 and day 7. A striking difference was higher remyelination capacity in the cerebral cortex, which seems to be supported by microglia dominance.

2021-02-23 | GSE167274 | GEO

Microglia regulate basal cerebral blood flow and neurovascular coupling through ectonucleotidase CD39

Project description:Microglia tightly interact with brain capillaries and regulate blood brain barrel permeability in pathological conditions. However, it is still unknown whether and how microglia regulate CBF in homeostatic condition. Here we show microglia directly regulate cerebral blood flow (CBF) and neurovascular coupling. Conditional knockout of microglial CD39 resulted in CBF hyper perfusion, reduced ATP induced CBF increase, impaired neurovascular coupling by whisker stimulation and reduced whisker stimulation induced adenosine increase in barrel cortex. Out data suggest that microglia is an important player for CBF regulation.

2023-07-01 | GSE223314 | GEO

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