Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TNFα and α-synuclein fibrils differently regulate human astrocyte immune reactivity and impair mitochondrial respiration

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE166771 | GEO | 2021/02/16

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

TNFα and α-synuclein fibrils differently regulate human astrocyte immune reactivity and impair mitochondrial respiration

Project description:TNFα and α-synuclein fibrils differently regulate human astrocyte immune reactivity and impair mitochondrial respiration

| PRJNA701924 | ENA

α-Synuclein Preformed Fibrils Bind to β-Neurexins and Impair β-Neurexin-Mediated Presynaptic Organization.

Project description: Not available

| S-EPMC10093570 | biostudies-literature

REV-ERB-alpha and -beta coordinately regulate astrocyte reactivity and proteostatic function.

Project description: Not available

| S-EPMC12867698 | biostudies-literature

Mitochondrial Respiration in Human Colorectal and Breast Cancer Clinical Material Is Regulated Differently.

Project description: Not available

| S-EPMC5525093 | biostudies-literature

Alpha-synuclein fibrils induce budding of mitochondrial-derived vesicles

Project description:α-synuclein (α-syn) aggregation is a hallmark of synucleinopathies, a class of neurodegenerative disorders such as Parkinson’s disease (PD). Several lines of evidence indicate the involvement of mitochondria in the disease pathology. Despite extensive study, the link between α-syn aggregation and mechanisms of mitochondrial toxicity remains not fully understood. Using high-resolution imaging with electron microscopy, we examined SH-SY5Y cells exposed to α-syn fibrils vs control cells with a focus on mitochondria. We found that upon exposure to α-syn fibrils, mitochondria cristae structure gets defects, and mitochondria enhance the budding of mitochondrial-derived vesicles (MDVs). MDV formation reflects an evolutionarily conserved mechanism reminiscent of bacterial outer membrane vesicle biogenesis. Structural proteomics analysis by mass spectrometry corroborates this microscopy observation by identifying changes in multiple proteins that regulate cristae structure, MDV formation, and trafficking. Our results suggest that α-syn may promote MDV generation, and support an important link between α-syn and mitochondria which will be important for future mechanistic studies. The processes we detected could be of interest for diagnostics and potential therapeutic interventions.

2026-06-29 | PXD078690 | Pride

Oral respiration modulates sensory and cognitive brain potentials differently than nasal respiration

Project description: Not available

| S-EPMC12340021 | biostudies-literature

TNFα and IL-1β modify the miRNA cargo of astrocyte shed extracellular vesicles to regulate neurotrophic signaling in neurons.

Project description: Not available

| S-EPMC5838212 | biostudies-literature

Mitochondrial glutamine transporter SLC1A5_var, a potential target to suppress astrocyte reactivity in Parkinson's Disease.

Project description: Not available

| S-EPMC9646772 | biostudies-literature

Nrf2 activation attenuates the early suppression of mitochondrial respiration due to the α-synuclein overexpression.

Project description: Not available

| S-EPMC6138761 | biostudies-literature

REV-ERB-alpha and -beta coordinately regulate astrocyte reactivity and proteostatic function

Project description:The molecular circadian clock is a ubiquitous transcriptional-translational feedback loop that regulates CNS function, glial responses, and neurodegenerative pathology. The druggable nuclear receptors REV-ERB-ɑ (gene: Nr1d1) and REV-ERB-.Beta. (gene: Nr1d2) are components of the core circadian clock. REV-ERB proteins regulate neuroinflammatory responses, synaptic pruning, and protein aggregation, though the cell type-specific effects and relative compensatory effects of REV-ERB-ɑ AND -.Beta. in the brain are unknown. To study the CNS functions of REV-ERBs, we developed mouse lines with global or astrocyte-specific, conditional knockout of both REV-ERB-ɑ and -.Beta.. We demonstrate that inducible post-natal global deletion of REV-ERB-ɑ and -.Beta. in vivo results in robust spontaneous astrocyte activation and increases gene expression of disease-relevant pathways such as protein catabolism, complement, and oxidative stress. Furthermore, in vivo astrocyte-specific deletion of REV-ERB-ɑ/-.Beta. recapitulates the spontaneous astrocyte activation phenotype seen in global REV-ERB-ɑ/-.Beta. KO mice, as well as in mice with deletion of key core clock gene Bmal1, indicating that REV-ERBs regulate astrocyte activation in a cell-autonomous manner downstream of the core circadian clock. REV-ERB-ɑ/-.Beta. repress transcription of Stat3 in the brain, and deletion of REV-ERBs in astrocytes induces increased astrocytic STAT3 expression and downstream STAT3-mediated gene changes, a mechanistic link to the astrocyte reactivity shift. This astrocyte activation phenotype decreases alpha-synuclein pathology in an in vivo model of Parkinson’s Disease-related alpha-synucleinopathy and increases astrocytic protein uptake and degradation in vitro. This study therefore provides insight into astrocyte function and could elucidate novel regulatory mechanisms that are candidates for therapeutic manipulation through modulating REV-ERB activity.

2026-01-14 | GSE293026 | 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