Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Aβ suppresses oligodendrocyte differentiation in vivo or vitro via inflammatory activation and cytoskeletal contraction.

ABSTRACT: Aβ disrupts oligodendrocyte lineage cells through a dual mechanism inflammatory activation and cytoskeletal compromise leading to maturation blockade and hypomyelination independent of axonal damage. These findings position oligodendrocyte dysfunction as a key component of AD white matter pathology and identify potential therapeutic targets.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE324555 | GEO | 2026/03/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Aβ suppresses oligodendrocyte differentiation in vivo or vitro via inflammatory activation and cytoskeletal contraction.

Project description:Aβ suppresses oligodendrocyte differentiation in vivo or vitro via inflammatory activation and cytoskeletal contraction.

| PRJNA1435787 | ENA

m6A mRNA methylation is essential for oligodendrocyte maturation and CNS myelination

Project description:Oligodendrocytes are responsible for myelin formation and axonal trophic support in the vertebrate CNS. While a number of factors have been discovered that regulate oligodendrocyte lineage progression, the exact molecular mechanisms involved in this process remain unclear. Emerging studies have shown that N6-methyladenosine (m6A), the most common internal RNA modification of mammalian mRNA, plays a critical role in various developmental processes. In this study, we demonstrate that oligodendrocyte lineage progression is accompanied by changes in m6A modification on numerous transcripts. In vivo conditional inactivation in oligodendrocyte lineage cells of an essential m6A writer component, METTL14, results in decreased oligodendrocyte numbers and CNS hypomyelination, although oligodendrocyte precursor cell (OPC) numbers are normal. In vitro Mettl14 ablation disrupts post-mitotic oligodendrocyte maturation. In addition, Mettl14 ablation has distinct effects on OPC and oligodendrocyte transcriptomes. Together, our findings indicate that dynamic RNA methylation plays a critical regulatory role in oligodendrocyte development and CNS myelination.

2020-01-01 | GSE136496 | GEO

Functional characterization of DNA methylation in the oligodendrocyte lineage [RNASeq_development]

Project description:Myelination in the CNS is modulated by interplay between transcription factors and recruitment of chromatin modifying enzymes. Using a network built from genome-wide DNA methylation and transcriptomic profiling of sorted oligodendrocyte lineage cells that integrates oligodendrocyte-specific ChIP-Seq data, we defined a crucial role of DNA methylation in coordinating the transition between progenitor cell cycle arrest and oligodendrocyte differentiation. We further identified DNA methyltransferase 1 (DNMT1) as key regulator of oligodendrocyte survival at this transition point, as we detected severe and extensive developmental hypomyelination only in Olig1cre/+;Dnmt1flox/flox but not in Olig1cre/+;Dnmt3aflox/flox mice or in Cnpcre/+;Dnmt1flox/flox. This phenotype was characterized by decreased expression of genes regulating myelination and lipid metabolism â despite the hypomethylation observed at these genetic loci Â â and upregulation of cell cycle and DNA-damage pathways. Therefore DNMT1 is a nodal point regulating proliferation, survival, and differentiation in the oligodendrocyte lineage, and is critical for cell number regulation in the developing brain. mRNA profiles of FAC-sorted P2 Pdgfra::GFP and P18 Plp1-GFP purified cell samples from mouse brains were generated by RNA-sequencing, in triplicate, using Illumina HiSeq 2000.

2016-04-14 | E-GEOD-66029 | biostudies-arrayexpress

Functional characterization of DNA methylation in the oligodendrocyte lineage [ERRBS]

Project description:Myelination in the CNS is modulated by interplay between transcription factors and recruitment of chromatin modifying enzymes. Using a network built from genome-wide DNA methylation and transcriptomic profiling of sorted oligodendrocyte lineage cells that integrates oligodendrocyte-specific ChIP-Seq data, we defined a crucial role of DNA methylation in coordinating the transition between progenitor cell cycle arrest and oligodendrocyte differentiation. We further identified DNA methyltransferase 1 (DNMT1) as key regulator of oligodendrocyte survival at this transition point, as we detected severe and extensive developmental hypomyelination only in Olig1cre/+;Dnmt1flox/flox but not in Olig1cre/+;Dnmt3aflox/flox mice or in Cnpcre/+;Dnmt1flox/flox. This phenotype was characterized by decreased expression of genes regulating myelination and lipid metabolism â despite the hypomethylation observed at these genetic loci Â â and upregulation of cell cycle and DNA-damage pathways. Therefore DNMT1 is a nodal point regulating proliferation, survival, and differentiation in the oligodendrocyte lineage, and is critical for cell number regulation in the developing brain. Genome wide DNA methylation profiles of FAC-sorted P2 Pdgfra::GFP and P18 Plp1-GFP purified cell samples from mouse brains were generated by ERRBS analysis, in duplicate, using Illumina HiSeq 2000.

2016-04-14 | E-GEOD-66028 | biostudies-arrayexpress

Impact of Major Facilitator Superfamily Domain containing 2a (Mfsd2a) mediated lipid transport on oligodendrocyte lineage development at single cell level.

Project description:Mfsd2a is involved in transport of essential fatty acids such as docosahexaenoic acid (DHA) from the periphery across blood brain barrier (BBB) into the brain parenchyma. Loss of Mfsd2a in humans leads to microcephaly and hypomyelination. The significance of lipid species transported by Mfsd2a on oligodendrocyte lineage development is not known. Using OPC specific deletion of Mfsd2a (2aOKO) in mice we found that OPC cell state, differentiation and oligodendrocytes maturation is disrupted resulting in hypomyelination compared to 2afl/fl controls. Single cell RNAsequencing analysis was performed on total oligodendrocyte population from postnatal mouse brain using Ribo-TRAP mouse lines that labels complete oligodendrocyte lineage with GFP fluorescence to understand the influence of Mfsd2a on oligodendrocyte development.

2023-05-17 | GSE211879 | GEO

Oligodendrocyte degeneration triggers the formation of inflammatory brain lesions

Project description:Here, we investigated whether cuprizone-induced oligodendrocyte apoptosis is sufficient to trigger peripheral immune cell recruitment into the forebrain. We show that early cuprizone-induced white matter lesions display a striking similarity to early MS lesions, i.e., oligodendrocyte degeneration, microglia activation and absence of lymphocytes. Such early cuprizone lesions are sufficient to trigger peripheral immune cell recruitment. The lesions are characterized by discontinuation of the perivascular glia limitans, focal axonal damage, and perivascular astrocyte pathology. Time course studies showed that the severity of cuprizone-induced lesions positively correlates with the extent of peripheral immune cell recruitment. Furthermore, results of genome-wide array analyses suggest that moesin is integral for early microglia activation in cuprizone and MS lesions. This study underpins the significance of brain-intrinsic degenerative cascades for immune cell recruitment and, in consequence, MS lesion formation.

2021-09-07 | GSE119672 | GEO

TMT-based proteomics analysis of optic nerve lysates from oligodendrocyte-specific Kir4.1 knockout mice

Project description:To study the role oligodendroglial Kir4.1 in regulating axonal energy metabolism, oligodendrocyte-specific Kir4.1 knockout mice and their littermate controls were used; optic nerve lysates were prepared for subsequent TMT-based proteomics.

2024-01-30 | PXD046207 | Pride

Functional characterization of DNA methylation in the oligodendrocyte lineage [RNASeq_development]

Project description:Myelination in the CNS is modulated by interplay between transcription factors and recruitment of chromatin modifying enzymes. Using a network built from genome-wide DNA methylation and transcriptomic profiling of sorted oligodendrocyte lineage cells that integrates oligodendrocyte-specific ChIP-Seq data, we defined a crucial role of DNA methylation in coordinating the transition between progenitor cell cycle arrest and oligodendrocyte differentiation. We further identified DNA methyltransferase 1 (DNMT1) as key regulator of oligodendrocyte survival at this transition point, as we detected severe and extensive developmental hypomyelination only in Olig1cre/+;Dnmt1flox/flox but not in Olig1cre/+;Dnmt3aflox/flox mice or in Cnpcre/+;Dnmt1flox/flox. This phenotype was characterized by decreased expression of genes regulating myelination and lipid metabolism – despite the hypomethylation observed at these genetic loci – and upregulation of cell cycle and DNA-damage pathways. Therefore DNMT1 is a nodal point regulating proliferation, survival, and differentiation in the oligodendrocyte lineage, and is critical for cell number regulation in the developing brain.

2016-04-14 | GSE66029 | GEO

Functional characterization of DNA methylation in the oligodendrocyte lineage [ERRBS]

Project description:Myelination in the CNS is modulated by interplay between transcription factors and recruitment of chromatin modifying enzymes. Using a network built from genome-wide DNA methylation and transcriptomic profiling of sorted oligodendrocyte lineage cells that integrates oligodendrocyte-specific ChIP-Seq data, we defined a crucial role of DNA methylation in coordinating the transition between progenitor cell cycle arrest and oligodendrocyte differentiation. We further identified DNA methyltransferase 1 (DNMT1) as key regulator of oligodendrocyte survival at this transition point, as we detected severe and extensive developmental hypomyelination only in Olig1cre/+;Dnmt1flox/flox but not in Olig1cre/+;Dnmt3aflox/flox mice or in Cnpcre/+;Dnmt1flox/flox. This phenotype was characterized by decreased expression of genes regulating myelination and lipid metabolism – despite the hypomethylation observed at these genetic loci – and upregulation of cell cycle and DNA-damage pathways. Therefore DNMT1 is a nodal point regulating proliferation, survival, and differentiation in the oligodendrocyte lineage, and is critical for cell number regulation in the developing brain.

2016-04-14 | GSE66028 | GEO

PKC-dependent MYRF dysregulation links Aβ pathology to oligodendrocyte, myelin and cognitive alterations in Alzheimer’s disease

Project description:PKC-dependent MYRF dysregulation links Aβ pathology to oligodendrocyte, myelin and cognitive alterations in Alzheimer’s disease

| PRJEB105554 | ENA

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