Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ScRNA seq analysis on immune cells isolated from nGD mice brain

ABSTRACT: We observed significant changes in gene expression between Wt and nGD brain. nGD brains are highly enriched for immune infiltrates, both microglia and immune infiltrates are activated in nGD brains. Through scRNA seq we identified that, microglia specific Gba deletion lead to higher activation and expression of DAM signature genes compared to control mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE207766 | GEO | 2022/07/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA seq analysis on immune cells isolated from nGD mice brain

Project description:We observed significant changes in gene expression between Wt and nGD brain. nGD brains are highly enriched for immune infiltrates, both microglia and immune infiltrates are activated in nGD brains. Through scRNA seq we identified that, microglia specific Gba deletion lead to higher activation and expression of DAM signature genes compared to control mice.

2022-07-13 | GSE207765 | GEO

scRNA seq analysis on immune cells isolated from nGD mice brain

Project description:scRNA seq analysis on immune cells isolated from nGD mice brain

| PRJNA857039 | ENA

RNA and scRNA seq analyses on immune cells isolated from nGD mice brain

Project description:RNA and scRNA seq analyses on immune cells isolated from nGD mice brain

| PRJNA857038 | ENA

Gene expression profiling of brain tissue from neuronopathic Gaucher disease mouse model of PG9VN, PG9V and wild type mice

Project description:To understand the intrinsic link between PGRN and Gba D409V mutation dosage in regulating lysosomal function and disease pathogenesis, we generated nGD model of GbaD409V/D409V and loss of PGRN (Grn-/-), termed PG9V that displayed typical neuronopathic GD (nGD). With decreasing the dose of Gba D409V, i.e., D409V/Null, in Grn KO mice (Grn-/-;GbaD409V/Null, PG9VN) led to much earlier onset and more severe neurodegenerative nGD than PG9V mice. To explore the correlation between the Gba mutation dosage and both neurodegeneration and inflammation, as well as to attain molecular insights into the underlying brain pathology in PG9VN mice, we performed bulk RNA sequencing analysis on 7.5-month-old PG9VN, PG9V and WT brain tissues containing thalamus, hypothalamus and midbrain, the predominant regions displaying the neuroinflammation and neurodegeneration. Gene Ontology (GO) analysis classified similar molecular pathways were altered in both PG9V and PG9VN mice. The heightened dysregulation of these pathways may be a contributing factor to the more severe disease phenotypes observed in PG9VN mice. This dysregulation appears to be controlled by a threshold effect related to Gba dosage.

2024-09-03 | GSE250051 | GEO

Single cell RNA-seq identifies a unique microglia type associated with Alzheimer’s disease [ChIP]

Project description:Alzheimer's disease (AD) is a detrimental neurodegenerative disease with no effective treatments. Due to cellular heterogeneity, the roles of immune cell subsets in AD onset and progression are poorly understood. By transcriptional single cell sorting, we comprehensively map all immune populations in wild type and AD–transgenic (Tg-AD) mouse brains. We describe a novel microglia type associated with neurodegenerative diseases (DAM) and identify the markers, spatial-location, and pathways associated with these cells. Immunohistochemical staining of mice and human brain slices showed DAM with intracellular/phagocytic Aβ particles. Single cell analysis of DAM in Tg-AD and Trem2-/- Tg-AD revealed that the DAM program is activated in a two-step process. Activation is initiated in a Trem2 independent manner which involves down-regulation of microglia checkpoints, followed by activation of a Trem2-dependent program. These data identify a unique microglia-type, which may have important implications for future treatment of AD and other neurodegenerative diseases.

2017-06-12 | GSE98970 | GEO

Single cell RNA-seq identifies a unique microglia type associated with Alzheimer’s disease [RNA]

2017-06-12 | GSE98969 | GEO

Gene expression of brain cells from wild type and Gba flox/flox; Nestin-Cre mice

Project description:To investigate neuronopathic Gaucher disease brain cell gene expression, we established Gba flox/flox; Nestin-Cre mice and performed scRNA sequencing of whole brain cells from these and wild type mice. Unbiased clustering analysis revealed that most remarkable change between wild type and Gba flox/flox; Nestin-Cre mice was the appearance of an activated microglia cluster, which exclusively expressed Tnf. Our further study elucidated the mechanism by which activated microglia and TNF contribute to Gaucher disease pathology.

2023-02-03 | GSE202929 | GEO

Senescence-Induced Immune Remodeling Facilitates Metastatic Adrenal Cancer in a Sex-Dimorphic Manner [scRNA-seq]

Project description:Using single-cell RNA-sequencing (scRNA-seq), we characterize diverse immune cell infiltrates that remodel the tissue microenvironment following senescence activation in female Znrf3 cKO mice.

2023-04-03 | GSE201126 | GEO

Proximity labeling proteomics reveals Kv1.3 potassium channel immune interactors in microglia.

Project description:Microglia are resident immune cells of the brain and regulate its inflammatory state. In neurodegenerative diseases, microglia transition from a homeostatic state to a state referred to as disease associated microglia (DAM). DAM express higher levels of proinflammatory signaling molecules, like STAT1 and TLR2, and show transitions in mitochondrial activity toward a more glycolytic response. Inhibition of Kv1.3 decreases the proinflammatory signature of DAM, though how Kv1.3 influences the response is unknown. Our goal was to establish the potential proteins interacting with Kv1.3 during transition to DAM. We utilized TurboID, a biotin ligase, fused to Kv1.3 to evaluate the potential interacting proteins with Kv1.3 via mass spectrometry in BV-2 microglia following TLR4-mediated activation. Electrophysiology, western blotting, and flow cytometry were used to evaluate Kv1.3 channel presence and TurboID biotinylation activity. We hypothesized that Kv1.3 contains domain-specific interactors that vary during a TLR4-induced inflammatory response, some of which are dependent on the PDZ-binding domain on the C-terminus. We determined that the N-terminus of Kv1.3 is responsible for trafficking Kv1.3 to the cell surface and mitochondria (e.g. NUNDC, TIMM50). Whereas, the C-terminus interacts with immune signaling proteins in an LPS-induced inflammatory response (e.g. STAT1, TLR2, and C3). There are 70 proteins that rely on the C-terminal PDZ-binding domain to interact with Kv1.3 (e.g. ND3, Snx3, and Sun1). Overall, we highlight that the Kv1.3 potassium channel functions beyond conducting the outward flux of potassium ions in an inflammatory context and that KV1.3 modulates activity of key immune signaling proteins, such as STAT1 and C3

2024-05-06 | PXD049433 | Pride

Deletion of Gba in neurons, but not microglia, causes neurodegeneration in a Gaucher mouse model

Project description:Gaucher disease, the most prevalent lysosomal storage disease, is caused by homozygous mutations at the GBA gene, which is responsible for encoding the enzyme glucocerebrosidase. Neuronopathic Gaucher disease is associated with microgliosis, astrogliosis, and neurodegeneration. However, the role that microglia, astrocytes, and neurons play in the disease remains to be determined. In the current study, we developed inducible, cell-type specific Gba KO mice to understand the individual impacts of Gba deficiencies on microglia and neurons. Gba was conditionally knocked out either exclusively in microglia or neurons, or throughout the body. These mouse models were developed using a tamoxifen-inducible Cre system, with tamoxifen administration commencing at weaning. Microglia-specific Gba KO mice showed no signs of disease. However, the neuron-specific Gba KO resulted in a shortened lifespan, severe weight loss, and ataxia. These mice also had significant neurodegeneration, microgliosis, and astrogliosis accompanied by the accumulation of glucosylceramide and glucosylsphingosine, recapitulating Gaucher disease-like symptoms. These surprising findings reveal that, unlike the neuron-specific Gba deficiency, microglia-specific Gba deficiency alone does not induce disease. The neuronal Gaucher disease mouse model, with a median survival of 16 weeks, may be useful for future studies of pathogenesis and the evaluation of therapies.

2024-10-02 | GSE247436 | 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