Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Siponimod ameliorates metabolic injury via the sphingosine1 phospohate receptor 5

ABSTRACT: we followed the hypothesis that Siponimod, a sphingosine-1 phosphate receptor modulator exerts protective effects by a direct modulation of glia cell function

ORGANISM(S): Mus musculus

PROVIDER: GSE213374 | GEO | 2022/09/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Altered gene expression in the neocortices and hippocampi of the adult S1P2-deficient and S1P3-deficient mice

Project description:Altered gene expression in the sphingosine 1-phosphate receptor 2 (S1P2)-deficient or sphingosine 1-phosphate receptor 3 (S1P3)-deficient brain. Keywords: genetic modification

2007-03-09 | GSE7191 | GEO

Vascular endothelial S1PR2 aggravates cardiac ischemia/reperfusion injury through triggering mitochondrial dysfunctions and endothelial pyroptosis via RHO/ROCK1/DRP1/NLRP3 pathway [heart]

Project description:Endothelial cell dysfunction plays an essential role in the process of cardiac ischemia-reperfusion (I/R) injury. Mitochondria damage, which can trigger inflammasome activation and subsequent pyroptosis, perturbs endothelial homeostasis, leading to aggravated cardiac I/R injury. Sphingosine 1-phosphate (S1P), a bioactive lipid molecule, exerts multifaceted effect on I/R injury via its different S1P receptors. However, the effect of EC-expressing S1P receptors on endothelial dysfunction, mitochondrial damage-induced inflammasome activation and consequent pyroptosis during cardiac I/R injury remain unclear. Our findings suggest a pivotal role of EC-expressing S1PR2 to control EC mitochondrial homeostasis and demonstrate that S1PR2-meidated mitochondrial dysfunction can trigger inflammasome activation and pyroptosis in ECs, which significantly influences inflammatory responses and heart injuries following I/R.

2024-07-25 | GSE245987 | GEO

Vascular endothelial S1PR2 aggravates cardiac ischemia/reperfusion injury through triggering mitochondrial dysfunctions and endothelial pyroptosis via RHO/ROCK1/DRP1/NLRP3 pathway [endothelial cells]

2024-07-25 | GSE245988 | GEO

Siponimod modulates the reaction of microglial cells to pro-inflammatory stimulation

Project description:Siponimod (Mayzent®), a sphingosine 1-phosphate receptor (S1PR) modulator which prevents lymphocyte egress from lymphoid tissues, is approved for the treatment of relapsing-remitting- and active secondary progressive multiple sclerosis. It can cross the blood-brain-barrier (BBB) and selectively binds to S1PR1 and S1PR5 expressed by several cell populations of the central nervous system (CNS) including microglia. To investigate wether Siponimod modulates the genetic signature of inflammed microglia, we performed a transcriptome analyses of primary rat microglial cells stimulated with LPS and With or Without Siponimod.

2022-11-02 | GSE216804 | GEO

Transcription profiling of mouse neocortices and hippocampi from adult S1P2-deficient and S1P3-deficient mice

Project description:Altered gene expression in the sphingosine 1-phosphate receptor 2 (S1P2)-deficient or sphingosine 1-phosphate receptor 3 (S1P3)-deficient brain. Experiment Overall Design: The S1P2-deficient mice suffer from spontaneous/sporadic seizures during 4-7 weeks of age. The S1P3 deficient mice do not show such seizures. The 8-week-old mice were sacrificed for sample preparation. Neocortices and hippocampi were isolated from wild-type, S1P2-deficient, and S1P2-deficient mice (n=10, 5, and 10, respectively).

2008-06-15 | E-GEOD-7191 | biostudies-arrayexpress

Title: Elevated SGPL1 expression increases metabolic rate and reduces survival in adrenocortical carcinoma patients

Project description:Sphingosine-1-phosphate lyase (SGPL1) catalyses the final step in sphingolipid metabolism (Figure 1), irreversibly degrading the lipid signalling molecule sphingosine-1-phosphate (S1P). Loss-of-function mutations in SGPL1 cause a spectrum of disorders, including primary adrenal insufficiency. Given loss of SGPL1 causes reduced steroidogenesis, while increased steroidogenesis is a hallmark of aggressive adrenocortical carcinomas (ACCs), we hypothesise increased SGPL1 expression might regulate ACCs. We identified a potential novel biomarker in ACCs, whereby increased SGPL1 expression correlates with reduced patient survival. We also saw similar correlation with other sphingolipid enzymes which diminish the ceramide pool, while those that replenish it confer a beneficial patient outcome. Increased SGPL1 expression in a cell model increased their resting proliferation and migration, although no effect on apoptosis was seen. There was a global decrease in the sphingolipid pool, possibly indicating increased flux through this pathway. RNAseq analysis identified an increase in expression of oxidative phosphorylation genes, and this correlated with an increase in basal and maximal glycolysis and oxidative phosphorylation. Finally, we showed that the increase in proliferation in the OE cells is dependent on the presence of metabolic substrates which may be used for anabolism and/or the production of ATP.

2022-12-08 | GSE190177 | GEO

Expression profiling of human mesoangioblasts indicates that S1P induces differentiation towards smooth muscle cells

Project description:cDNA microarray study of human mesoangioblasts treated with 1 µM sphingosine 1-phosphate (S1P) at 6 and 24 h.

2011-05-01 | GSE17596 | GEO

Effects of Sphingosine 1-Phosphate on Gene Expression in C3H10T1/2 Cells via RNA-seq

Project description:RNA sequencing was used to evaluate genes regulated in C3H10T1/2 cells by the G protein-coupled receptor agonist sphingosine 1-phosphate.

2021-01-02 | GSE108681 | GEO

Cell-penetrant SELENOT mimetic protects dopaminergic neurons and ameliorates motor function

Project description:Parkinson’s disease (PD) is a neurodegenerative disorder characterized by motor dysfunction for which there is an unmet need for better treatment options. Although oxidative stress is a common feature of neurodegenerative diseases, notably PD, there is currently no efficient therapeutic strategy able to tackle this system-wide pathophysiological process. Based on our previous observations of the potent antioxidant and neuroprotective activity of SELENOT, a vital thioredoxin-like selenoprotein, we designed the small peptide PSELT from its redox active site in order to determine its potential polyfunctional activity in PD models. PSELT proved to site in order to be protective for neurotoxin-treated dopaminergic neurons and fibers against oxidative stress determine its potential polyfunctional activity in PD models. PSELT proved to be protective for neurotoxin-treated dopaminergic neurons and fibers against oxidative stress and cell death. We demonstrate that PSELT is cell-permeable and acts in different subcellular compartments of dopaminergic neurons where oxidative stress exerts its deleterious effects. This protective activity prevented neurodegeneration and restored phosphorylated tyrosine hydroxylase levels, leading to improved motor skills in rodent models of PD

2021-02-08 | GSE151808 | GEO

Project description:Commensal Lactobacillus Suppress Colon Tumorigenesis and Progression by Modulation of Sphingosine 1-Phosphate Signaling in Mice

| PRJNA807432 | 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