Browse
Submit Data
Databases
API
Help

Dataset Information

9 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of mouse mast cells treated with an antagonist for recepter CRTH2, compound A alone and with CRTH2 ligands, antigen, BW868c and dexatheasone

ABSTRACT: These samples are part of a study in which we demonstrate that mast cells express the receptor CRTH2, which is the target for our antagonist compound compound A. We want to examine whether there are differences in RNA expression when the mast cells are treated with the ligands of CRTH2 - PGD2 and DK-PGD2 - compared to no treatment. Also, we want to see if pretreating the cells with compound A can block or change differences in RNA expression induced by either DK-PGD2 or PGD2. The study also looks at Ige loaded cells exposed to antigen and dexamethasone, and cells treated with BW868c - a a highly selective DP receptor antagonist.

ORGANISM(S): Mus musculus

SUBMITTER: Narimene Lekmine

PROVIDER: E-TABM-498 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of lung from mice challenged with cockroach antigen and treated with a drug, compound A

Project description:A highly specific and potent small molecule antagonist of CRTH2 (chemoattractant receptor) was used to investigate the role of this PGD2 receptor in a chronic model of airway inflammation and the underlying immune responseThis is a mouse asthma model which uses CRA (cockroach antigen) All the mice in this study were immunized with CRA followed by aerosolized CRA as a challenge. There are 3 experimental groups in this study. One cohort of mice was "simply" challenged (samples 1-3), another cohort was challenged and received the drug vehicle (samples 4-9), and the third cohort received the drug compound A prior to antigen challenge (samples 10-14). Each sample is from a different mouse. Following the aero-challenge, the mice were sacrificed, lungs harvested and RNA was made for gene expression analysis.

2009-07-07 | E-TABM-499 | biostudies-arrayexpress

Effects of group III phospholipase A2 deficiency in mast cells on fibroblast-directed maturation of mast cells in vitro

2013-03-09 | GSE44980 | GEO

Mast Cell Maturation is Driven via a Novel Group III Phospholipase A2-Prostaglandin D2-DP1 Receptor Paracrine Axis

Project description:Microenvironment-based alterations in mast cell phenotypes influence the susceptibility to anaphylaxis, yet the mechanisms underlying proper maturation of mast cells toward an anaphylaxis-sensitive phenotype are incompletely understood. Here we report that PLA2G3, a mammalian homolog of anaphylactic bee venom phospholipase A2, regulates this process. PLA2G3 secreted from mast cells is coupled with fibroblastic lipocalin-type PGD2 synthase (L-PGDS) to provide PGD2, which facilitates mast cell maturation via PGD2 receptor (DP1). Mice lacking PLA2G3, L-PGDS or DP1, mast cell-deficient mice reconstituted with PLA2G3- or DP1-null mast cells, or mast cells cocultured with L-PGDS-ablated fibroblasts exhibited impaired mast cell maturation and anaphylaxis. Thus, we describe a lipid-driven PLA2G3-L-PGDS-DP1 loop that drives mast cell maturation. Mast cell maturation; immature and mature bone marrow-derived mast cells (BMMCs); Four-condition experiment (mature BMMCs vs immature BMMCs, Pla2g3M-bM-^@M-^S/M-bM-^@M-^S vs Pla2g3+/+); 3 replicates of Pla2g3+/+ BMMCs, 4 replicates of Pla2g3M-bM-^@M-^S/M-bM-^@M-^S BMMCs, 4 replicates of Pla2g3+/+ cocultured BMMCs, 3 replicates of Pla2g3M-bM-^@M-^S/M-bM-^@M-^S cocultured BMMCs

2013-03-09 | E-GEOD-44980 | biostudies-arrayexpress

Transcription profiling of mouse skin treated with ovalbumin to induce atopic dermatitus and then treated with a test drug or ramatroban or dexamethasone

Project description:A highly specific and potent small molecule antagonist of CRTH2 (chemoattractant receptor) was used to investigate the role of this Prostaglandin D2 (PGD2) receptor in chronic models of cutaneous inflammation and the underlying immune response. These RNA samples are from mice that were in a chronic (50 day) model of atopic dermatitis. Each mouse had a section of back skin patched with a gauze, and the RNA was from the patched area of skin; the control mice had the gauze soaked in PBS, whereas all the other test mice had the gauze soaked in ovalbumin dissolved in PBS. The ovalbumin acts as an allergen and induces the experimental atopic dermatitis. The six groups of mice that received the OVA patch were treated in different ways:some received just the drug vehicle during the OVA patching, others received the test drug (compound A) at 3 different concentrations: 10 mg/kg 1 mg/kg and 0.1 mg/kg. Two other cohorts received positive control drugs: ramatroban and dexamethasone .Each different sample represents a different animal.

2009-06-25 | E-TABM-505 | biostudies-arrayexpress

RNA-seq of human type 2 innate lymphoid cells (ILC2) stimulated with PGD2 or PGD2 metabolites (Δ12PGJ2, Δ12PGD2, 15-deoxyΔ12,14PGD2, 9α,11β-PGF2) with or without the selective DP2 antagonist fevipiprant

Project description:ILC2s were isolated from peripheral blood of four patients with atopic asthma. ILC2s were stimulated with PGD2 and four PGD2 metabolites (Δ12PGJ2, Δ12PGD2, 15-deoxyΔ12,14PGD2, 9α,11β-PGF2) with or without the selective DP2 antagonist fevipiprant. Total RNA was sequenced, and differentially expressed genes (DEG) were identified by DeSeq2.

2023-12-26 | E-MTAB-13623 | biostudies-arrayexpress

Transcription profiling of mouse skin with atopic dermatitus after treatment with a CRTH2 antagonist or dexamethasome for 24 hours

Project description:The role of CRTH2 (chemoattractant receptor) in a murine allergic contact inflammation model of human Atopic Dermatitis was investigated.This an acute model of atopic dermatitis in which a CRTH2 antagonist (compound A) and a positive control drug (dexamethasone, Dex) were evaluated. The experimental protocol was as follows:the mice first had their stomach area shaved, and either FITC (Fluorescein isothiocyanate) or the vehicle FITC is dissolved in (acetone:DBPTH) is applied to the skin on day 1 and day 2. The mouse generated an immune response to FITC and made specific antibodies. Six days later, the mouse was challenged, which consisted of putting FITC on the right ear and the vehicle w/o FITC (acetone:DBPTH) on the left ear. After 24 hrs. the thickness of each ear was measured, and to gauge the level of swelling/inflammation, the thickness of the left ear was compared to the FITC treated right ear. To assess the ability of the drug to block inflammation, the difference in R/L ear thickness were comparedfrom the mice that received FITC on the right ear, and drug vehicle (FITC/Vehicle group) to the group that received FITC on the right ear and either compound A (FITC/compound A) or dexamethasone (FITC/Dex). The control group only had vehicle (acetone:DBPTH) applied to the stomach area on days 1 & 2, and vehicle applied to both the right and left ears at the time of challenge. They also received the drug vehicle solution. The control animals did not mount a response to the vehicle (acetone:DBPTH) and did not have an increase in ear thickness compared to untreated animals.

2009-07-17 | E-TABM-521 | biostudies-arrayexpress

Transcription profiling of mouse skin with atopic dermatitus after treatment with a CRTH2 antagonist or dexamethasome for 4 hours

2009-06-23 | E-TABM-523 | biostudies-arrayexpress

Transcription profiling of mouse skin after treatement with Fluorescein isothiocyanate reveals FITC-induced skin inflammation is CRTH2 dependent - 8 hour drug treatment

2009-06-27 | E-TABM-522 | biostudies-arrayexpress

The Effect of Steroid and ERa agonism on Th2 cells

Project description:Allergic asthma is a T helper 2 (Th2) cell-associated inflammatory disease, driven by cytokines such as IL-4, IL-5, and IL-13. Th2 cells express the G-protein-coupled receptor CRTh2, a receptor for prostaglandin D2 (PGD2) that influences Th2 function and survival. Inhaled glucocorticosteroids are the primary treatment of allergic asthma and improve asthma symptoms by inhibiting Th2 cytokine production. Women are more likely than men to have severe asthma and to have symptoms requiring a hospital visit. These findings lead us to consider a mechanism by which female sex hormones could influence Th2 cell response to glucocorticosteroid. Using whole-mRNA sequencing, we examined gene expression in primary Th2 cells following exposure to glucocorticosteroids (0.1µM) in the presence or absence of an estrogen mimic, PPT (10µM).

2022-10-19 | GSE132699 | GEO

Activation of IL5R and CRTH2 on Human Eosinophils Elicit a Similar Molecular Response and Reveal a Synergistic Effect

Project description:Eosinophils represent key cells driving inflammatory processes in asthma and eosinophilic esophagitis (EoE). Eosinophils migration and activation in disease is orchestrated by a myriad of molecules among which prostaglandin D2, the cognate ligand of CRTH2, and interleukin 5 play a crucial role. In clinical studies with CRTH2 antagonists and anti-IL-5 antibodies, a reduction of the number of eosinophils in disease tissue of asthma and EoE patients was demonstrated, validating the pharmacological effects on eosinophils migration. In contrast, activation of eosinophils through IL5 or CRTH2 receptor has not been studied to the same extent. Understanding the molecular CRTH2 and IL5 activation bias in disease would provide a better assessment of pharmacological intervention, or the need for a combination therapy, to block eosinophils efficiently. We performed gene expression profiling studies with isolated human eosinophils to compare the molecular signatures of CRTH2 and IL5 receptor activation. Furthermore we employed gene set enrichment analysis to query the eosinophils activation bias in asthma and EoE. We observed that activation of CRTH2 and IL5 on human eosinophils shared a large part of the molecular response but also present distinct molecular signatures. Remarkably, FADS1, involved in the synthesis of prostaglandin D2, was identified as a specific CRTH2-induced gene that is counter-regulated by IL5, potentially representing a feedback loop between CRTH2 and IL5 receptor. In silico use of the identified gene signatures and FADS1 demonstrated an enrichment of the IL5 activation signature in lung tissue of asthma patients, whereas esophagus tissue of EoE patients presented a CRTH2 bias.

2018-07-25 | GSE75142 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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