Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis of microglia depleted and non-depleted hippocampus tissue

ABSTRACT: Sepsis-associated encephalopathy is a common complication during systemic inflammation. Microglia are key player in this process. For a better understanding we compared hippocampal tissue following sepsis induction of microglia depleted and non-depleted mice. We show an overall reduction of inflammatory response in the hippocampus of microglia depleted animals.

ORGANISM(S): Mus musculus

PROVIDER: GSE198861 | GEO | 2022/10/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptome analysis of microglia at day 3 and 20 following sepsis induction

Project description:Sepsis-associated encephalopathy is a common complication during systemic inflammation. Microglia are key player in this process. For a better understanding we compared isolated microglia from mice at day 3 and day 20 following induction of polymicrobial sepsis. We found a long-lasting inflammatory response of microglia following sepsis.

2022-10-17 | GSE198862 | GEO

Development of gene expression signatures for BV-2 microglia activation in the background of mild hypothermia

Project description:Sepsis associated encephalopathy (SAE), a common complication of sepsis, seriously affect the prognosis and quality of life to sepsis patients. Microglia activation is vital to the neuroinflammation and the pathology of SAE. Mild hypothermia, that a useful procedure in the treatment of traumatic brain injuries, was found to suppress microglia activation. In present study, in vitro cultured BV-2 microglial cells stimulated with LPS was employed as the model of microglia activation. The altered signitures of lncRNAs, circRNAs and mRNAs of LPS exposure and mild hypothermia were arrayed by using the Agilent ceRNA Microarray Chip.

2021-11-10 | GSE171696 | GEO

Transcriptome analysis of microglia depleted and non-depleted hippocampus tissue

Project description:Transcriptome analysis of microglia depleted and non-depleted hippocampus tissue

| PRJNA817198 | ENA

Gene expression profiles of endothelium, microglia and oligodendrocytes in hippocampus of post-stroke depression rat at single cell resolution

Project description:Post-stroke depression (PSD) is a common but severe mental complication after stroke. However, the cellular and molecular understanding of PSD is still yet to be illustrated. In current study, we prepared PSD rat model (MD) via unilateral middle cerebral artery occlusion (MCAO) and chronic stress stimulation (DEPR), and isolated hippocampal tissues for single cell sequencing of 10x Genomics Chromium. This study characterized the single cell expression profile of hippocampal PSD, and unmask the differential expressed genes of endothelium, microglia and oligodendrocytes, emphasizing the crosstalk among them to provide theoretical basis for the in-depth mechanism research and drug therapy of PSD.

2023-05-24 | GSE232936 | GEO

N-acetyltransferase 10 mediates cognitive dysfunction through the acetylation of GABABR1 mRNA in sepsis-associated encephalopathy.

Project description:Sepsis-associated encephalopathy (SAE) is a critical neurological complication of sepsis and represents a crucial factor contributing to high mortality and adverse prognosis in septic patients. This study explore the influence of NAT10-mediated mRNA acetylation on SAE and the mechanisms underlying cognitive dysfunction in this context. SAE was induced in C57BL/6 J male mice through cecal ligation and puncture (CLP) surgery. In vivo, we observed a significant increase in NAT10 expression in the excitatory neurons of the hippocampal the dentate gyrus (DG) in CLP mice, and this change was accompanied by a trend toward an increase in mRNA acetylation. Specific knockout of Nat10 in neurons led to an improvement in cognitive dysfunction in septic mice. Proteomic analysis and RNA immunoprecipitation and real-time quantitative polymerase chain reaction (RIP-qPCR) revealed GABABR1 as a crucial downstream target of NAT10. Nat10 deletion reduced GABABR1 expression, subsequently weakening inhibitory postsynaptic currents in hippocampal DG neurons. Additionally, RNA sequencing (RNA-seq) revealed an increase in hippocampal inflammation post-CLP, characterized by the excessive activation of microglia and the release of inflammatory mediators. These factors were linked to the increased NAT10 expression in neurons. Treatment with PLX3397, a microglia depleting agent, resulted in a reduction in NAT10 and GABABR1 expression in neurons, which correlated with improvements in cognitive dysfunction induced by SAE. Taken together, our findings revealed that after CLP, NAT10 in neurons of the hippocampal DG region promotes GABABR1 expression by acetylating its mRNA, leading to cognitive dysfunction. These findings provide new insights into the molecular pathogenesis of SAE and suggest potential therapeutic targets for addressing cognitive deficits in septic patients.

2024-08-13 | GSE253309 | GEO

Single Cell RNAseq of the hippocampus after RSD following microglia depletion

Project description:Chronic stress is associated with anxiety and cognitive impairment. Repeated social defeat (RSD) in mice induces anxiety-like behavior driven by microglia and the recruitment of inflammatory monocytes to the brain. Nonetheless, it is unclear how microglia communicate with other cells to modulate the physiological and behavioral responses to stress. Using single-cell (sc)RNAseq, novel stress-associated microglia were identified in the hippocampus and defined by RNA profiles of cytokine/chemokine signaling, cellular stress, and phagocytosis. Microglia depletion with a CSF1R antagonist (PLX5622) attenuated the stress-associated profile of leukocytes, endothelia, and astrocytes. Furthermore, RSD-induced social withdrawal and cognitive impairment were microglia dependent, but social avoidance was microglia independent. Furthermore, single-nuclei (sn)RNAseq showed robust responses to RSD in hippocampal neurons that were both microglia dependent and independent. Notably, stress-induced CREB, oxytocin, and glutamatergic signaling in neurons were microglia dependent. Collectively, these stress-associated microglia influenced transcriptional profiles in the hippocampus linked to social and cognitive deficits.

2024-10-02 | GSE275205 | GEO

Microglia mediate neurocognitive deficits by eliminating C1q tagged synapses in sepsis-associated encephalopathy

Project description:Microglia mediate neurocognitive deficits by eliminating C1q tagged synapses in sepsis-associated encephalopathy

| PRJNA817210 | ENA

Increased glucose uptake in hippocampus as a surrogate biomarker of metabolic reconfiguration of microglia in Alzheimer’s disease

Project description:Microglia is dynamically reprogrammed according to the progression of Alzheimer’s disease (AD). However, clinical translation into biomarker development for functional change in microglia has not been achieved. Here, we find the close association of the metabolic reconfiguration of microglia with increased hippocampal glucose uptake, which can be noninvasively estimated by [18F]fluorodeoxyglucose (FDG) positron emission tomography (PET). We found that increased FDG activity in the hippocampus of an AD mouse model depended on microglial uptake. Single-cell RNA-sequencing of the hippocampus showed the changes of glucose metabolism profiles including glucose transporters, glycolysis and oxidative phosphorylation mainly occurred in microglia. A subset of microglia with high glucose transporters with defective glycolysis and oxidative phosphorylation was increased according to disease progression. Furthermore, we also found a positive association between a soluble TREM2 of cerebrospinal fluid, a marker of microglial activation, and hippocampal FDG uptake as a human study. We identified a reconfiguration of microglial glucose metabolism in the hippocampus of AD and suggested a feasible imaging biomarker based on widely used FDG PET to reflect microglial metabolic profiles.

2021-09-08 | GSE150934 | GEO

Formation of Müller glia-derived progenitor cells in retinas depleted of microglia

Project description:Recent studies have demonstrated the complex coordination of pro-inflammatory signaling and reactive microglia/macrophage on the formation Müller glial-derived progenitor cells (MGPCs) intheretinas offish, birds and mice.We generated scRNA-seq libraries to identify transcriptional changes in Müller glia (MG) that result from the depletion of microglia from the chick retina. We found significant changes in different networks of genes in MG in normal and damaged retinas when the microglia are ablated. We identified a failure of MG to upregulate Wnt-ligands, Heparin binding epidermal growth factor (HBEGF), Fibroblast growth factor (FGF), retinoic acid receptors and genes related to Notch-signaling. Inhibition of GSK3β, to simulate Wnt-signaling, failed to rescue the deficit in formation of proliferating MGPCs in damaged retinas missing microglia. By comparison, application of HBEGF or FGF2 completely rescued the formation of proliferating MGPCs in microglia-depleted retinas. Similarly, injection of a small molecule inhibitor to Smad3 or agonist to retinoic acid receptors partially rescued the formation of proliferating MGPCs in microglia-depleted damaged retinas. According to scRNA-seq libraries, patterns of expression of ligands, receptors, signal transducers and/or processing enzymes to cell-signaling via HBEGF, FGF, retinoic acid and TGFβ are rapidly and transiently upregulated by MG after neuronal damage, consistent with important roles for these cell-signaling pathways in regulating the formation of MGPCs. We conclude that quiescent and activated microglia have a significant impact upon the transcriptomic profile of MG. We conclude that signals produced by reactive microglia in damaged retinas stimulate MG to upregulate cell signaling through HBEGF, FGF and retinoic acid, and downregulate signaling through TGFβ/Smad3 to promote the reprogramming on MG into proliferating MGPCs.

2023-09-14 | GSE242796 | GEO

RNAseq data of brain cortex from mice at d10 post-microglia depletion and non-depleted controls

Project description:Previous studies have reported that microglia depletion leads to impairment of synapse formation and these cells rapidly repopulate from CNS progenitors. However, the impact of microglia depletion and repopulation on the long-term state of the CNS environment has not been characterized. Here, we found by RNA-seq analysis that acute and synchronous microglia depletion results in a type 1-interferon inflammatory signature in degenerating somatosensory cortex in microglia-depleted mice. Transcriptomic and mass cytometry analysis of repopulated microglia demonstrates an interferon regulatory factor 7-driven activation state. Minocycline and anti-IFNAR1 antibody treatment attenuate the CNS type-1 interferon-driven inflammation and restore microglia homeostasis. Together, we found that acute microglia ablation induces a type-1 interferon activation state of grey matter microglia associated with acute neurodegeneration.

2018-06-08 | GSE115447 | 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