Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Octopamine metabolically reprograms astrocytes to confer neuroprotection against α-synuclein

ABSTRACT: Octopamine metabolically reprograms astrocytes to confer neuroprotection against α-synuclein

PROVIDER: PRJNA882845 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21660016.fastq.gz	Fastqsanger.gz
	SRR21660017.fastq.gz	Fastqsanger.gz
	SRR21660018.fastq.gz	Fastqsanger.gz
	SRR21660019.fastq.gz	Fastqsanger.gz
	SRR21660020.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 17

Similar Datasets

Octopamine metabolically reprograms astrocytes to confer neuroprotection against α-synuclein

Project description:Octopamine is a well-established invertebrate neurotransmitter involved in fight-or-flight responses. In mammals, its function was replaced by norepinephrine. Nevertheless, it is present at trace amounts and can modulate the release of monoamine neurotransmitters by a yet unidentified mechanism. Here, through a multidisciplinary approach utilizing in vitro and in vivo models of a-synucleinopathy, we uncovered an unprecedented role for octopamine in driving the conversion from toxic to neuroprotective astrocytes in the cerebral cortex by fostering aerobic glycolysis. Neuron-derived octopamine acts on astrocytes via a TAAR1-Orai1-Ca2+-calcineurinmediated signaling pathway to stimulate lactate secretion. Lactate uptake in neurons via the MCT2-calcineurin-dependent pathway increases ATP and prevents neurodegeneration. Pathological increases of octopamine caused by a-synuclein halts lactate production in astrocytes and short-circuits the metabolic communication to neurons. Our work provides a novel function of octopamine as a modulator of astrocyte metabolism and hence neuroprotection with implications to a-synucleinopathies.

2023-04-01 | GSE213875 | GEO

Crosslinking of Ly6a metabolically reprograms CD8 T cells for cancer immunotherapy.

Project description:Crosslinking of Ly6a metabolically reprograms CD8 T cells for cancer immunotherapy.

| PRJNA1139138 | ENA

Sirt2 Inhibition Reprograms T Cell Metabolism to Confer Superior Anti-Tumor Immunity

Project description:Sirt2 Inhibition Reprograms T Cell Metabolism to Confer Superior Anti-Tumor Immunity

| PRJNA635802 | ENA

A novel class of early responder T cells are indispensable for neuroprotection and functional recovery after ischemic stroke

Project description:We report that CD8+CD122+CD49dlow regulatory-like T cells (CD8+TRLs) are among the earliest lymphocytes to infiltrate mouse brain after ischemic stroke, temper inflammation, and confer neuroprotection.

2022-08-03 | GSE201054 | GEO

GHB analogs confer neuroprotection through specific interaction with the CaMKII hub domain

Project description:Ca2+/calmodulin-dependent protein kinase II alpha (CaMK2A) is an emerging drug target incerebral ischemia for which limited therapeutic options exist. Here we show that small-molecule analogs of the brain metabolite gamma-hydroxybutyric acid (GHB) afford neuroprotection via interaction specifically with the CaMK2A hub domain. Identification of CaMK2A as the GHB analog target was achieved by homogenate photoaffinity labeling followed by quantitative proteomics

2021-07-22 | PXD019679 | Pride

Schistosoma mansoni infection metabolically reprograms the myeloid lineage in a mouse model of metabolic disease

Project description:Schistosoma mansoni infection metabolically reprograms the myeloid lineage in a mouse model of metabolic disease

| PRJNA648919 | ENA

The responses of astrocytes stimulated by extracellular a-synuclein

Project description:Abnormal neuronal aggregation of a-synuclein is implicated in the development of Parkinson’s disease. Glial cells also show extensive a-synuclein pathology and are thought to contribute to disease progression. However, the mechanism that produces the glial a-synuclein pathology and the interaction between neurons and glia in the disease-inflicted microenvironment remain unknown. Here, we show that in neuronal cells misfolded a-synuclein proteins are selectively translocated into vesicles, leading to exocytosis of the aggregated forms. More importantly, our data demonstrate that astrocytes take up the neuron-derived a-synuclein aggregates and produce a-synuclein inclusions similar to the ones found in human brains. This uptake is paralleled by changes in the gene expression profile reflecting an inflammatory response. These results suggest that astroglial a-synuclein pathology is produced by cell-to-cell transmission of neuronal a-synuclein aggregates. This transmission step is thus an important mediator of pathogenic glial responses and could qualify as a new therapeutic target. To determine how astrocytes respond to extracellular a-synuclein, gene expression profiles were established and analyzed for nearly 22,000 rat genes using the Illumina RatRef-12 Expression BeadChip. Total RNA was isolated from astrocytes exposed for 6h or 24h to conditioned medium from cultures of a-synuclein or lacZ expressing cells.

2010-01-11 | E-GEOD-11574 | biostudies-arrayexpress

Pro-survival Lipid Sphingosine-1-Phosphate Metabolically Reprograms T cell to Limit its Anti-Tumor Activity

Project description:Pro-survival Lipid Sphingosine-1-Phosphate Metabolically Reprograms T cell to Limit its Anti-Tumor Activity

| PRJNA531482 | ENA

Maternal slimming reprograms metabolic gene expression in mice offspring

Project description:This SuperSeries is composed of the following subset Series: GSE40471: Maternal slimming reprograms metabolic gene expression in mice offspring (NimbleGen expression) GSE40477: Maternal slimming reprograms metabolic gene expression in mice offspring (NimbleGen methylation) GSE40478: Maternal slimming reprograms metabolic gene expression in mice offspring (mRNA-Seq) Refer to individual Series

2012-08-30 | E-GEOD-40479 | biostudies-arrayexpress

The responses of astrocytes stimulated by extracellular a-synuclein

2010-01-12 | GSE11574 | GEO