Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PEST-domain-enriched tyrosine phosphatase and glucocorticoids as regulators of mast cell signalling

ABSTRACT: PEST-domain-enriched tyrosine phosphatase (PEP) is a cytoplasmic protein tyrosine phosphatase that regulates immune cell functions, including mast cell functions. Using bone marrow derived mast cells (BMMCs) from PEP+/+ and PEP-/- mice, RNA-seq data showed that dinitrophenol (DNP) - activated PEP-/- BMMCs have misregulated gene expression, with some cytokine/chemokine genes (eg.TNFα, IL13, CSF2) showing reduced gene expression in the dinitrophenol (DNP) - activated PEP-/- BMMCs compared to (DNP)-activated PEP+/+ BMMCs. Also, the ability of the glucocorticoid dexamethasone (Dex) to negatively regulate DNP - induced COX-2 gene expression in PEP-/- BMMCs was inhibited compared to the PEP+/+ BMMCs.

ORGANISM(S): Mus musculus

PROVIDER: GSE108972 | GEO | 2018/01/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

MicroRNA profiling of mouse bone marrow-derived mast cells during mucosal differentiation and IgE-mediated activation

Project description:The aim of this study was to investigate microRNA expression pattern and its functional relevance on the commitment toward mucosal differentiation and on IgE-mediated activation of mast cells. To identify microRNA genes the expression of which change during the differentiation and activation of murine primary mast cells in vitro, the putative committed progenitors (c-kit+ cells isolated on day 6 from differentiating cultures), immature mast cells (BMMC), mucosal-type mast cells (MMC), and IgE-activated mast cells were compared by Agilent microRNA array. RNA was isolated by miRNeasy (Qiagen) from: 1) c-kit+ cells, isolated from differentiating cultures (in the presence of IL3 and SCF) derived from the bone marrow using MACS column purification, 2) immature BMMCs obtained by cultivation of bone marrow cells in the presence of IL3 and SCF for 4 weeks, 3) mucosal-type mast cells by additional differentiation of immature BMMCs for 5 days by supplementation of IL9 and TGFbeta, and 4) activated mast cells by presensitization with anti-DNP IgE followed by IgE-crosslinking by DNP-antigen challenge for 2 hours. Agilent microRNA microarray was run on these experimental groups. Four biological replicates were included in every experimental group.

2011-01-01 | E-GEOD-24321 | biostudies-arrayexpress

Pac1+/+ versus Pac1-/- BMMCs_IgE-DNP 2 h

Project description:Bone marrow-derived mast cells were differentiated over 4-6 weeks using bone marrow from Pac-1+/+ and Pac1-/- littermate mice. Cell purity was 99% c-kit and Fc epsilon receptor positive as assessed by flow cytometry. Cells were stimulated by Fc epsilon receptor crosslinking using IgE-DNP/HSA for sensitization for 18 hours and DNP-HSA antigen for crosslinking for 2 hours. Gene transcript abundance was determined and scaled to 150 using alogorithms in MicroArray Analysis Suite Software 5.0 (Affymetrix). Keywords: Cpmparison of Pac-1+/+ and Pac-1-/- activated BMMCs

2006-01-10 | GSE3994 | GEO

Nano-silica particles synergistically IgE-mediated mast cell activation

Project description:To deeply investigate the details of the nano-SiO2 effects, we examined the gene expression profile alterations after nano-SiO2 treatment in BMMCs. The difference analysis between the groups showed that 285 genes were significantly expressed after treatment with nano-SiO2. Compared with the blank group, both nano-SiO2 exposure and DNP-HSA stimulation increased the expression of genes related to the MAPK signaling pathway in mast cells to varying degrees.

2022-07-05 | GSE206630 | 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

Expression data from activated and non-activated NTAL knockout, wild type and knockdown bone marrow derived mast cells

Project description:Non-T cell activation linker (NTAL, also called Lab or LAT2) is a transmembrane adaptor protein involved in the high affinity IgE receptor (FcεRI) signaling in mast cells. Studies with bone marrow-derived mast cells (BMMCs) from NTAL-/- mice indicated that NTAL is a negative regulator of FcεRI signaling. In contrast, depletion of NTAL by RNA interference in human or rat mast cells suggested its positive regulatory role. To determine whether compensatory developmental alterations are responsible for the observed discrepancies, we compared FcεRI-mediated signaling events in BMMCs isolated from NTAL-/- mice or BMMCs of wild type in which NTAL expression was decreased by RNA interference. We found that when compared to corresponding controls, NTAL-deficient cells, both knockouts (KOs) and knockdowns (KDs), exhibited enhanced degranulation, calcium mobilization, tyrosine phosphorylation of linker for activation of T cells (LAT) and ERK, depolymerization of filamentous actin and chemotaxis. These data indicate that NTAL in mouse BMMCs is a negative regulator of FcεRI signaling, independently of compensatory developmental alterations. To gain more insight into NTAL function, we examined gene expression profiles of resting and antigen-activated BMMCs with NTAL KO or KD and corresponding controls and identified several genes that were more than 1.8-fold differentially expressed in resting and FcεRI-activated NTAL-deficient cells, when compared to wild-type controls. We provide evidence that at least some of these genes could be involved in regulation of cholesterol-dependent events in chemotaxis towards antigen.

2014-08-26 | GSE40731 | GEO

PEST-domain-enriched tyrosine phosphatase and glucocorticoids as regulators of mast cell signalling

Project description:PEST-domain-enriched tyrosine phosphatase and glucocorticoids as regulators of mast cell signalling

| PRJNA429265 | ENA

Effect of deficiency of Elk4 on transcriptome changes in murine bone marrow derived mast cells upon FcϵRI mediated activation

Project description:The proliferative potential of mast cells after activation for 3-4h was found to be decreased, which suggests that mast cell degranulation and cell proliferation are differentially regulated. ELK4, a member of the ternary complex factor (TCF) subfamily of Ets transcription factors, is one of the downstream effectors of MAPK signaling that is critical for cell proliferation. And Elk4 has been identified to be vital for macrophage activation in response to zymosan and the transcriptional response to 12-O-tetrade canoyl phorbol-13-acetate (TPA) stimulation in fibroblast. However, the effect of ELK4 on the mast cell transcriptional response to FcϵRI and GPCR mediated activation and its potential functional significance in mast cells remain unclear. Here, We characterised the transcriptional program downstream of FcϵRI signalling using IgE-DNP/HSA stimulation by RNA-seq. The investigation of the transcriptional response was performed using murine bone marrow derived mast cells(BMMCs) from different animals: (i) wild type mice, (ii) Elk4 heterozygous mice, (iii) Elk4 knockout mice. Overall, our study identifies a new physiological role of the transcription factor ELK4 in mast cell proliferation and activation.

2023-07-12 | GSE236014 | GEO

Identification of genes involved in the anti-inflammatory effects of berberine in DNP-activated mouse MC/9 mast cells

Project description:Atopic dermatitis is a common chronic inflammatory skin disease characterized by infiltration of inflammatory cells, extensive pruritus and a clinical course of symptomatic flares and remissions. Berberine (BER), a naturally occurring isoquinoline alkaloid, has many pharmacological effects including inhibition of protein synthesis, cell cycle arrest, and anti-inflammatory activities. However, a detailed molecular mechanism underling the anti-inflammatory action of BER in inflammatory cells is unclear. Here, to identify genes involved in the anti-inflammatory effects of BER in DNP-activated mouse MC/9 mast cells, global-scale gene expression analysis was carried out using a GeneChipÃÂ® system. Mouse MC/9 mast cells were treated with BER (10 microM), DNP (anti-DNP IgE, Sigma; 500 microg/ml) or a combination of BER and DNP. Total RNA samples were prepared from the cells, and quality of the RNA was analyzed using a Bioanalyzer 2100. Gene expression was analyzed by an Affymetrix GeneChipÃÂ® system with a Mouse Genome 430 2.0 array. Sample preparation for array hybridization was carried out as described in the manufacturerÃ¢ÂÂs instructions.

2015-12-22 | E-GEOD-76202 | biostudies-arrayexpress

Transcription profiling of mouse IgE/antigen-activated mast cells stimulated with TIM-3

Project description:TIM-3 is known to be expressed on dendritic cells, monocytes, melanoma cells, mast cells and on activated Th1 cells. In activated Th1 cells, stimulating TIM-3 by one of its ligands, galectin-9, leads to apoptosis and thus it plays a central role in terminating Th1-type immune responses. Interestingly, in IgE/antigen-activated mast cells TIM-3 enhances the production of IL-13 and IL-4. To get a more complete picture about the gene expression changes induced by TIM-3 in mast cells, in vitro differentiated mouse immature mast cells were stimulated by an agonist anti-TIM-3 antibody and IgE-sensitized mouse immature mast cells were activated by antigen and an agonist anti-TIM-3 antibody for 2 or 16 hours (overnight). Experiment Overall Design: Bone marrow cells were differentiated in RPMI + 10% FCS + 5 ng/ml mouse IL-3 + 40 ng/ml mouse SCF for >4 weeks. The purity of the cell cultures was >90% at this time point (FcERIa+/c-kit+ cells). These in vitro-differentiated immature mast cells were then treated by either control goat IgG or an agonist anti-mouse TIM-3 antibody (RnD Systems, 15 ug/ml for 2 or 16 hours). For the IgE/antigen-activated mouse mast cells, these in vitro-differentiated immature mast cells were sensitized by 5 ug/ml anti-DNP IgE (Sigma) for 1 hour and then treated with 100 ng/ml DNP-HSA (antigen, Sigma) and either control goat IgG or an agonist anti-mouse TIM-3 antibody (RnD Systems, 15 ug/ml) for 2 or 16 hours. The anti-TIM-3 samples were labeled by Cy5 and they were compared to the Cy3-labeled, goat IgG controls in a dual-color, paired experimental setup. The Agilent Whole Mouse Genome 4x44K expression microarray kit and Dual-Color Protocol version 5.5 were used in the experiments.

2009-10-15 | E-GEOD-14438 | biostudies-arrayexpress

Mast cell expression data from murine aryl hydrocarbon receptor (AhR) null, AhR_d and normal control mice

Project description:We found that AhR, a unique chemical sensor, is critical in controlling mast cell differentiation, growth and function in vitro and in vivo. This study seeks to further the understanding of the mechanisms of how AhR control mast cell homeostasis. Three different batches of bone marrow derived mast cells (BMMCs) from AhR null, AhR_d and normal control mice were cultured in 30% WEHI-3-conditioned medium. BMMCs were purified by negative selection with MicroBeads (Miltenyi Biotec) after 4 weeks in culture. 99% BMMCs were FcM-NM-5RI+ c-kit+ CD49b- by flow cytometry analysis. The cells were further rested in cytokine free medium for 4h. Subsequently, total RNA was collected. Gene expression profiling was performed on total RNA from mast cells using Illumina SentrixM-BM-. Murine Ref8_v2_R3 BeadChips. Details of the design and the gene signatures found are given in the paper associated with this GEO Series: Yufeng Zhou, Hui-Ying Tung, Ying-Ming Tsai, Shih-Chang Hsu, Hui-Wen Chang, Hirokazu Kawasaki, Hsiao-Chun Tseng, Beverly Plunkett, Peisong Gao, Chih-Hsin Hung, Becky M. Vonakis, and Shau-Ku Huang. M-bM-^@M-^\Aryl hydrocarbon receptor controls murine mast cell homeostasisM-bM-^@M-^], Blood 2013 Mar 5 [Epub ahead of print]

2013-04-01 | E-GEOD-44715 | biostudies-arrayexpress

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