Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Neuronal EphB1 induces STAT3 activation in astrocytes, which is impaired in ALS models

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

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE102904 | GEO | 2017/09/01

SECONDARY ACCESSION(S): PRJNA399190

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Neuronal EphB1 induces STAT3 activation in astrocytes, which is impaired in ALS models [Mm]

Project description:Astrocyte responses to neuronal injury may be beneficial or detrimental to neuronal recovery, but the mechanism that determines these different responses are poorly understood. Transcriptional analysis showed that EphB1 induces a protective inflammatory signature in astrocytes, which is distinct from the response evoked by interleukin (IL)-6, which is known to have both pro- and anti-inflammatory properties. We demonstrate that this beneficial EphB1 induced signaling pathway is disrupted in astrocytes derived from human induced pluripotent stem cells (iPSC) of amyotrophic lateral sclerosis (ALS) patients.

2017-09-01 | GSE102903 | GEO

Neuronal EphB1 induces STAT3 activation in astrocytes, which is impaired in ALS models [Hs]

2017-09-01 | GSE102902 | GEO

Neuronal EphB1 induces STAT3 activation in astrocytes, which is impaired in ALS models

Project description:Neuronal EphB1 induces STAT3 activation in astrocytes, which is impaired in ALS models

| PRJNA399190 | ENA

Sporadic ALS Astrocytes Induce Neuronal Degeneration In Vivo.

Project description:Astrocytes from familial amyotrophic lateral sclerosis (ALS) patients or transgenic mice are toxic specifically to motor neurons (MNs). It is not known if astrocytes from sporadic ALS (sALS) patients cause MN degeneration in vivo and whether the effect is specific to MNs. By transplanting spinal neural progenitors, derived from sALS and healthy induced pluripotent stem cells (iPSCs), into the cervical spinal cord of adult SCID mice for 9 months, we found that differentiated human astrocytes were present in large areas of the spinal cord, replaced endogenous astrocytes, and contacted neurons to a similar extent. Mice with sALS but not non-ALS cells showed reduced non-MNs numbers followed by MNs in the host spinal cord. The surviving MNs showed reduced inputs from inhibitory neurons and exhibited disorganized neurofilaments and aggregated ubiquitin. Correspondingly, mice with sALS but not non-ALS cells showed declined movement deficits. Thus, sALS iPSC-derived astrocytes cause ALS-like degeneration in both MNs and non-MNs.

| S-EPMC5390239 | biostudies-literature

Neuronal activity induces glutathione metabolism gene expression in astrocytes.

Project description:The idea that astrocytes provide support for neurons has a long history, but whether neurons play an instructive role in these processes is poorly understood. To address this question, we co-culture astrocytes with genetically labeled neurons, permitting their separation by flow cytometry, and test whether the presence of neurons influences the astrocyte transcriptome. We find that numerous pathways are regulated in the co-cultured astrocytes, in a time-dependent matter coincident with synaptic maturation. In particular, the induction of glutathione metabolic genes is prominent, resulting in increased glutathione production. We show that the induction of the glutathione pathway is mediated by astrocytic metabotropic glutamate receptors. Using a candidate approach, we identify direct binding of the nuclear factor E2-related factor, NRF2, to several of the induced genes. Blocking nuclear accumulation of astrocytic NRF2 abolishes neuron-induced glutathione gene induction and glutathione production. Our results suggest that astrocyte transcriptional and metabolic profiles are tightly coupled to the activity of neurons, consistent with the model that astrocytes dynamically support healthy brain function.

| S-EPMC6185788 | biostudies-literature

miR-424 induces COP1 silencing and STAT3 activation in prostate cancer: a novel miRNA-dependent axis driving tumor progression

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-03-09 | GSE60371 | GEO

PIKFYVE Inhibition Mitigates Disease in Models of Diverse Forms of ALS

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-12-18 | GSE221017 | GEO

Reactive astrocytes in ALS models display dysregulated intron retention

Project description:Reactive astrocytes are implicated in Amyotrophic Lateral Sclerosis (ALS), although the mechanisms controlling reactive transformation are unknown. We show that decreased intron retention (IR) is common to human induced pluripotent stem cell (hiPSC)-derived astrocytes carrying VCP, C9orf72 and SOD1 ALS-causing mutations as well as astrocytes stimulated to undergo reactive transformation. Notably, transcripts with decreased IR and increased expression are overrepresented in reactivity processes including cell-adhesion, stress-response, and immune-activation. We examined astrocyte translatome sequencing (TRAP-seq) from a SOD1 mouse model, which revealed a significant number of transcripts with reduced IR in ALS are upregulated in translation. Using nucleo-cytoplasmic fractionation of VCP astrocytes coupled with mRNA sequencing and proteomics, we identify that decreased IR in nuclear-detained transcripts is associated with increased cytoplasmic expression of genes and proteins encoding regulators of reactivity - indicating nuclear-to-cytoplasmic translocation and translation of spliced reactivity-related transcripts. These results provide novel insights into the molecular factors controlling the reactive transformation of ALS astrocytes.

2021-10-25 | GSE160133 | GEO

Autophagy induction enhances TDP43 turnover and survival in neuronal ALS models.

Project description:Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) have distinct clinical features but a common pathology--cytoplasmic inclusions rich in transactive response element DNA-binding protein of 43 kDa (TDP43). Rare TDP43 mutations cause ALS or FTD, but abnormal TDP43 levels and localization may cause disease even if TDP43 lacks a mutation. Here we show that individual neurons vary in their ability to clear TDP43 and are exquisitely sensitive to TDP43 levels. To measure TDP43 clearance, we developed and validated a single-cell optical method that overcomes the confounding effects of aggregation and toxicity and discovered that pathogenic mutations shorten TDP43 half-life. New compounds that stimulate autophagy improved TDP43 clearance and localization and enhanced survival in primary murine neurons and in human stem cell-derived neurons and astrocytes harboring mutant TDP43. These findings indicate that the levels and localization of TDP43 critically determine neurotoxicity and show that autophagy induction mitigates neurodegeneration by acting directly on TDP43 clearance.

| S-EPMC4106236 | biostudies-literature

Post-transcriptional remodelling is temporally deregulated during motor neurogenesis in human ALS models

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-05-31 | GSE98290 | GEO