Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Viktor Molnár

PROVIDER: E-GEOD-24321 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

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

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.

2011-01-01 | GSE24321 | GEO

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

Project description: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.

2018-01-31 | GSE108972 | GEO

Notch signaling promotes differentiation of mouse mucosal mast cells

Project description:Intestinal mucosal mast cells are critically involved in the development of food-induced allergic disorders. However, factors that induce differentiation of mucosal mast cells in the intestinal mucosa are largely unknown. To identify factors involved in mucosal mast cell differentiation, we compared the gene expression profiles between mucosal mast cells isolated from the small intestine and bone marrow-derived mast cells cultured in the presence of TGF-Î² or Notch ligand. Mucosal mast cells were isolated from the small intestine of naÃ¯ve BALB/c mice by flow cytometry. Bone marrow-derived mast cells (BMMCs) were generated by culturing BALB/c bone marrow cells with murine interleukin-3 and stem cell factor for 3-4 weeks, and then cells were cultured for 6 days in the presence or absence of TGF-Î² or Delta-like 1 (Dll1), which is a Notch ligand. Total RNAs extracted from these cells were processed and hybridized to Affymetrix GeneChips.

2016-06-15 | E-GEOD-80139 | 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

Stem cell factor programs the mast cell activation phenotype

Project description:Mast cells, activated by antigen via the high affinity receptor for IgE (FcεRI), release an array of pro-inflammatory mediators that contribute to allergic disorders such as asthma and anaphylaxis. The KIT ligand, stem cell factor (SCF), is critical for mast cell expansion, differentiation and survival, and, under acute conditions, enhances mast cell activation. However, extended SCF exposure in vivo conversely protects against fatal antigen-mediated anaphylaxis. In investigating this dichotomy, we identified a novel mode of regulation of the mast cell activation phenotype through SCF-mediated programming. We found that mouse bone marrow-derived mast cells chronically exposed to SCF displayed a marked attenuation of FcεRI-mediated degranulation and cytokine production. The hypo-responsive phenotype was not a consequence of altered signals regulating calcium flux or protein kinase C, but of ineffective cytoskeletal reorganization, with evidence implicating a down-regulation of expression of the Src kinase Hck. Collectively, these findings demonstrate a major role for SCF in the homeostatic control of mast cell activation with potential relevance to mast cell-driven disease and the development of novel approaches for the treatment of allergic disorders. Mouse bone marrow-derived mast cells were treated with IL3, IL3+IL33, or IL3+SCF. Six replicates each.

2012-05-01 | E-GEOD-35332 | 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

Mediating effects of miR-155 on the FceRI signaling responses of mast cells

Project description:MicroRNA 155 (miR-155) has been shown to regulate the gene expression of important players of physiological and pathological processes, like hematopoietic lineage differentiation, immunity and inflammation, viral infections, cancer and cardiovascular diseases, among others. Degranulation is an event in which mast cells, upon activation of the FceRI, release their granule content rich in vasoactive amines, proteases and TNFa. Additionally activation of the receptor promotes de novo synthesis of cytokines, chemokines and growth factors. Analysis of bone marrow derived mast cells (BMMC) deficient in miR-155 showed a significant increase in FceRI mediated degranulation and in the release of cytokines like TNFa, IL-6 and IL-13. In addition miR 155-/- mice presented higher anaphylaxis reactions compared to WT mice. Gene expression analysis of BMMC was performed in order to identify intermediaries of FceRI mediated degranulation under the control of miR-155. The results indicate that miR-155 regulates negatively the expression of the regulatory subunits of the kinase PI3Kgamma, Pik3r5 (p101) and Pik3r6 (p84, p87PIKAP), involved in Ca+ influx and degranulation. Total RNA from 3 independent cultures of WT and miR-155-/- BMMC treated with anti-DNP IgE and 20 ng/ml DNP-HSA for 1hr were used to performed gene expression analysis using the Affymetrix GenechipM-BM-. Mouse Gene 1.0 ST

2014-03-20 | E-GEOD-56030 | 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

Transcriptional heterogeneity of mast cells and basophils upon activation.

Project description:Mast cells and basophils are developmentally related cells whose activation is a hallmark of allergy. Functionally, mast cells and basophils overlap in their ability to produce several mediators, including histamine and granule proteases, but studies have increasingly demonstrated non-redundant roles. To characterize the transcriptional heterogeneity of mast cells and basophils upon their activation, we performed large-scale comparative microarrays of murine bone marrow–derived mast cells (BMMCs) and basophils (BMBs) at rest, upon an adaptive-type activation (IgE crosslinking), or upon an innate-type activation (IL-33 stimulation). Hierarchical clustering demonstrated that BMMCs and BMBs shared specific activation-associated transcriptional signatures but differed in others, both between cell type and between activation mode. In BMMCs, IgE crosslinking upregulated 785 genes including Egr2, Ccl1, and Fxyd6, while IL-33 stimulation induced 823 genes including Ccl1, Egr2, and Il1b. Focused bioinformatics pathway analysis demonstrated that IgE activation aligned with processes such as oxidative phosphorylation, angiogenesis, and the p53 pathway. The IL-33–activated transcriptome was enriched in genes commonly altered by NF-B in response to TNF, by IL-6 via STAT3, and in response to IFN. Furthermore, BMBs activated via IgE crosslinking selectively induced immune response genes Ccl1, Il3, and Il2 compared to IL-33–stimulated BMBs. Principal-component analysis revealed key cell- and activation-specific clustering. Overall, our data demonstrate that mast cells and basophils have cell- and activation-specific transcriptional responses and suggest that context-specific gene networks and pathways may shape how the immune system responds to allergens and innate cytokines.

2017-03-17 | GSE96696 | GEO

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