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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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

ORGANISM(S): Mus musculus

SUBMITTER: Silvia Bulfone-Paus

PROVIDER: E-GEOD-56030 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2014-03-20 | GSE56030 | 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

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

MAZR and mast cells

Project description:Mast cells are known to be the key players in type I hypersensitivity reactions in humans and mice. They are critically involved in the development of allergic rhinitis, allergic asthma and systemic anaphylaxis. In this study we investigated the role of the transcriptional regulator MAZR in mast cells by comparing the expression profile of mast cells generated from wild-type (MazrF/F) and MAZR-deficient (MazrF/F x Vav-iCre) bone marrow cells. Our results from the array data demonstrate that MAZR acts preferentially as a transcriptional repressor in mast cells.

2013-10-18 | E-MTAB-1816 | 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 microRNAs regulated by KIT signaling

Project description:Objective is to identify microRNAs regulated by KIT signaling in mast cells. miRNA profiles of murine bone marrow derived mast cells with and without SCF treatment were compared. In addition, miRNA profiles of the P815 mutant KIT cell line with and without the KIT inhibitor, imatinib, were compared. We identified miRNAs that were differentially regulated by KIT signals. Two systems were used to identify microRNAs regulated by KIT. RNA was collected from primary murine bone marrow derived mast cells (BMMC) treated and not treated with KIT ligand (SCF). In addition, RNA was harvested from the P815 (activating KIT mutation positive) cell line treated and not treated with the KIT inhibitor, imatinib. Samples were harvested after 24 hours of treatment

2011-01-25 | E-GEOD-26783 | biostudies-arrayexpress

Analysis of bone marrow derived mast cell transcriptomes in presence or absence of SialostatinL

Project description:Goal of this study was to compare transcriptional changes in stimulated mast cells in the absence or presence of sialostatinL mRNA profiles of 4 weeks old mast cells (BMMC derived from C57BL/6 mice ) stimulated for 24h with ionomycin in absence or presence of tick derived sialostatinL were generated by deep sequencing using Illumina HiSeq2000

2015-04-01 | E-GEOD-66966 | biostudies-arrayexpress

Transcription profiling of mouse bone marrow-derived mast cells were differentiated over 4-6 weeks using bone marrow from Pac-1+/+ and Pac1-/- littermate animals

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). Experiment Overall Design: Two genechips on independent mBMMC cultures was performed. The signal data of the .CEL files for the four Affymetrix 430A chips (2 Pac1+/+ and 2 Pac1â/â) were normalised using the RMA method 49. The ebayes function implemented in the version 1.3.12 of the Limma package (2003) of Bioconductor was used to analyse the data and P-values were adjusted for multiple testing. After conversion from logged values to the original intensities, the data was filtered to remove probe sets with mean, non-logged, intensities below 100. Transcripts with p-values less than 0.05 were considered different from Pac1+/+.

2008-06-12 | E-GEOD-3994 | biostudies-arrayexpress

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

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

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