Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Loss of PD-1 aggravates plaque pathology by disrupting microglial phagocytosis in APP/PS1 mice

ABSTRACT: Astrocytic secretion of soluble B7-H1 and subsequent engagement with microglial PD-1 regulates microglial clearance of Ab by modulating the expression of CD36.

ORGANISM(S): Mus musculus

PROVIDER: GSE77643 | GEO | 2021/12/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

SELENOK-Dependent CD36 Palmitoylation Regulates Microglial Functions and Aβ Phagocytosis

Project description:Amyloid-beta (Aβ) is a key factor in the onset and progression of Alzheimer's disease (AD). Selenium (Se) compounds show promise in AD treatment. Here, we reveal that selenoprotein K (SELENOK), a selenoprotein involved in immune regulation and potentially related to AD pathology, plays a critical role in microglial immune response, migration, and phagocytosis. In vivo and in vitro studies corroborate that SELENOK deficiency inhibits microglial Aβ phagocytosis, exacerbating cognitive deficits in 5xFAD mice, which are reversed by SELENOK overexpression. Mechanistically, SELENOK is involved in CD36 palmitoylation through DHHC6, regulating CD36 localization to microglial plasma membranes and thus impacting Aβ phagocytosis. CD36 palmitoylation is reduced in the brains of AD patients and mice. Se supplementation promotes SELENOK expression and CD36 palmitoylation, enhancing microglial Aβ phagocytosis and mitigating AD progression. We have identified the regulatory mechanisms from Se-dependent selenoproteins to Aβ pathology, providing novel insights into potential therapeutic strategies involving Se and selenoproteins.

2024-02-29 | GSE255034 | GEO

Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice.

Project description: Not available

| S-EPMC3528309 | biostudies-other

Transcriptional signature in microglia associated with Aβ plaque phagocytosis

Project description:The role of microglia cells in Alzheimer’s disease (AD) is well recognized, however their molecular and functional diversity remain unclear. Here we isolated amyloid plaque-containing (using labelling with methoxy–XO4, XO4+) and non-containing (XO4-) microglia from an AD mouse model. Transcriptomics analysis identified different transcriptional trajectories in ageing and AD mice. XO4+ microglial transcriptomes demonstrated dysregulated expression of genes associated with late onset AD. We further showed that the transcriptional program associated with XO4+ microglia from mice is present in a subset of human microglia isolated from brains of individuals with AD. XO4- microglia displayed transcriptional signatures associated with accelerated ageing and contained more intracellular post-synaptic material than XO4+ microglia, despite reduced active synaptosome phagocytosis. We identified HIF1α as potentially regulating synaptosome phagocytosis in vitro using primary human microglia, and BV2 mouse microglial cells. Together these findings provide insight into molecular mechanisms underpinning the functional diversity of microglia in AD.

2021-04-12 | PXD024731 | Pride

Deep cervical lymph node ligation aggravates AD-like pathology of APP/PS1 mice.

Project description: Not available

| S-EPMC8028636 | biostudies-literature

Transcriptional signature in microglia associated with Aβ plaque phagocytosis

2021-01-31 | GSE165306 | GEO

Complement C3 deficiency protects against neurodegeneration in aged plaque-rich APP/PS1 mice.

Project description: Not available

| S-EPMC6936623 | biostudies-literature

Particulate Matter Exposure Exacerbates Amyloid-β Plaque Deposition and Gliosis in APP/PS1 Mice.

Project description: Not available

| S-EPMC8100996 | biostudies-literature

Microglia - astrocyte cross-talk in the amyloid plaque niche of an Alzheimer’s disease mouse model as revealed by spatial transcriptomics (CosMx)

Project description:In this study, we characterize the transcriptomic alterations, cellular compositions, and signaling perturbations in the amyloid plaque niche in an AD mouse model using high-resolution spatial transcriptomics (CosMx and Stereo-seq). We discover a wide heterogeneity in the cellular composition of amyloid plaque niches, marked by an increase in microglial accumulation over time. We profile the alterations of glial cells as they are exposed to plaques, and conclude that the microglial response to plaques is consistent across different brain regions, while the astrocytic response is more heterogeneous. In turn, as the microglial density of plaque niches increases, astrocytes acquire a more neurotoxic phenotype and play a key role in inducing GABAergic signaling and decreasing glutamatergic signaling in neurons of the hippocampus. Taken together, we show that astrocytic signaling around plaque pathology is disrupted with increasing microglial density, which in turn induces an imbalance in synaptic signaling in neurons in the hippocampus.

2024-04-19 | GSE263791 | GEO

Gene expression from primary brain cell cultures and RNA mixtures.

Project description:Gene expression from primary neuronal, astrocytic, oligodendrocytic and microglial cultures, as well as from RNA mixtures thereof. Keywords: Primary cell cultures Primary neuronal, astrocytic, oligodendrocytic and microglial cultures (4 biological replicates of each), as well as RNA mixtures thereof (5 different mixing proportions, 2 independent replicates of each mixing proportion).

2010-12-01 | E-GEOD-19380 | biostudies-arrayexpress

Microglia - astrocyte cross-talk in the amyloid plaque niche of an Alzheimer’s disease mouse model as revealed by spatial transcriptomics (Stereo-seq Spatial Transcriptomics)

2024-04-19 | GSE263789 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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