Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A Cellular Atlas of the Down Syndrome Brain Identifies Accelerated Oligodendrocyte Precursor Cell Senescence

ABSTRACT: A Cellular Atlas of the Down Syndrome Brain Identifies Accelerated Oligodendrocyte Precursor Cell Senescence

PROVIDER: PRJNA936175 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23513804_1.fastq.gz	Fastqsanger.gz
	SRR23513804_2.fastq.gz	Fastqsanger.gz
	SRR23513805_1.fastq.gz	Fastqsanger.gz
	SRR23513805_2.fastq.gz	Fastqsanger.gz
	SRR23513806_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

A Cellular Atlas of the Down Syndrome Brain Identifies Accelerated Oligodendrocyte Precursor Cell Senescence

Project description:We performed single nucleus RNA-seq and single nucleus ATAC-seq on the cortex of Ts65Dn mouse model of Down Syndrome and euploid controls (wild types).

2023-09-14 | GSE225554 | GEO

Single-Nucleus Profiling Identifies Accelerated Oligodendrocyte Precursor Cell Senescence in a Mouse Model of Down Syndrome.

Project description:Down syndrome (DS), the most common genetic cause of intellectual disability, is associated with lifelong cognitive deficits. However, the mechanisms by which triplication of chromosome 21 genes drive neuroinflammation and cognitive dysfunction are poorly understood. Here, using the Ts65Dn mouse model of DS, we performed an integrated single-nucleus ATAC and RNA-sequencing (snATAC-seq and snRNA-seq) analysis of the adult cortex. We identified cell type-specific transcriptional and chromatin-associated changes in the Ts65Dn cortex, including regulators of neuroinflammation, transcription and translation, myelination, and mitochondrial function. We discovered enrichment of a senescence-associated transcriptional signature in Ts65Dn oligodendrocyte (OL) precursor cells (OPCs) and epigenetic changes consistent with a loss of heterochromatin. We found that senescence is restricted to a subset of OPCs concentrated in deep cortical layers. Treatment of Ts65Dn mice with a senescence-reducing flavonoid rescued cortical OPC proliferation, restored microglial homeostasis, and improved contextual fear memory. Together, these findings suggest that cortical OPC senescence may be an important driver of neuropathology in DS.

| S-EPMC10449487 | biostudies-literature

Investigation of Oligodendrocyte Precursor Cell Differentiation by Quantitative Proteomics

Project description:Oligodendrocytes, the myelinating cells of the central nervous system, are essential for correct brain function. They originate from oligodendrocyte precursor cells (OPCs) through a differentiation process which is only incompletely understood and impaired in a variety of demyelinating diseases. Better knowledge of this differentiation holds the promise to develop novel therapies for these disorders. We investigated the differentiation of rat oligodendrocyte precursor cells to oligodendrocytes in vitro. After confirmation of differentiation by immunohistochemical analysis using cell type-specific marker proteins, we conducted a quantitative proteomics study using tandem mass tags (TMT). We investigated four time points of differentiation covering early, intermediate, and late stages. Data analysis was perfomed using Mascot and Maxquant.

2019-06-21 | PXD012544 | Pride

Expression profiles in Chd7 knockdown oligodendrocyte precursor cells

Project description:Oligodendrocytes are generated from oligodendrocyte precursor cells (OPCs). Chd7 is ATP-dependent chromatin-remodeling enzyme. We performed microarray analysis to examine changes in gene expression between control and Chd7 knockdown OPCs. Results provide insight into the function of Chd7 in oligodendrocyte development.

2018-03-01 | GSE95347 | GEO

Transcriptome outcome of oligodendrocyte precursor cells following VCAM1 knockdown

Project description:Transcriptome outcome of rat oligodendrocyte precursor cells, which were knocked down with short-hairpin RNA (shRNA) for vascular cell adhesion molecule 1 (VCAM1)

2016-10-14 | GSE86862 | GEO

Single-cell transcriptomic analysis of human and mouse oligodendrocyte precursor cells

Project description:We report single cell gene expression analysis of human fetal and mouse postnatal oligodendrocyte precursor cells

2023-09-13 | GSE214086 | GEO

Reactive human iPSC astrocytes suppress oligodendrocyte precursor cell differentiation

Project description:Reactive human iPSC astrocytes suppress oligodendrocyte precursor cell differentiation

| PRJNA805526 | ENA

Quetiapine induces oligodendrocyte precursor cell differentiation by cholesterol biosynthesis

Project description:Quetiapine induces oligodendrocyte precursor cell differentiation by cholesterol biosynthesis

| PRJNA515864 | ENA

RNA-seq analysis for mRNA expression change in alpha-synclein fibril-treated cultured oligodendrocyte precursor cells

Project description:Glial cytoplasmic inclusion is the pathological hallmark of multiple system atrophy commonly observed as alpha-synulcien-positive aggregates within oligodendrocytes. We elucidated that preformed alpha-synulcien fibrils triggers multimerization and upsurge of endogenous alpha-synulcien in oligodendrocyte precursor cells which is attributable to insufficient autophagic proteolysis. To assess the functional influence of alpha-synuclein fibrils application on oligodendrocyte precursor cells, RNA-seq analysis was performed. The data revealed that alpha-synulcien fibrils interfered with numerous protein expressions associated with neuronal support and myelination.

2017-12-02 | GSE107582 | GEO

GDE3 regulates oligodendrocyte precursor proliferation via release of soluble CNTFRα

Project description:Oligodendrocyte development is tightly controlled by extrinsic signals; however, mechanisms that modulate cellular responses to these factors remain unclear. Six-transmembrane glycerophosphodiester phosphodiesterases (GDEs) are emerging as central regulators of cellular differentiation via their ability to shed glycosylphosphatidylinositol (GPI)-anchored proteins from the cell surface. We show here that GDE3 controls the pace of oligodendrocyte generation by negatively regulating oligodendrocyte precursor cell (OPC) proliferation. GDE3 inhibits OPC proliferation by stimulating ciliary neurotrophic factor (CNTF)-mediated signaling through release of CNTFRα, the ligand-binding component of the CNTF-receptor multiprotein complex, which can function as a soluble factor to activate CNTF signaling. GDE3 releases soluble CNTFRα by GPI-anchor cleavage from the plasma membrane and from extracellular vesicles (EVs) after co-recruitment of CNTFRα in EVs. These studies uncover new physiological roles for GDE3 in gliogenesis and identify GDE3 as a key regulator of CNTF-dependent regulation of OPC proliferation through release of CNTFRα.

2019-09-06 | GSE135819 | 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