Notch signaling promotes differentiation of mouse mucosal mast cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE80139 | GEO | 2016/06/15
SECONDARY ACCESSION(S): PRJNA318022
REPOSITORIES: GEO
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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-β or Notch ligand. Mucosal mast cells were isolated from the small intestine of naïve 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-β 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
Project description:The aim of the study was to find novel genes highly upregulated in mouse mucosal mast cells. To carry it out, differentiating progenitor cells were isolated on day4 of culturing and compared to mature mucosal mast cells obtained by day20. Keywords: cell differentiation stage comparison
2007-01-31 | GSE6192 | GEO
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
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
Project description:The aim of the study was to find novel genes highly upregulated in mouse mucosal mast cells. To carry it out, differentiating progenitor cells were isolated on day4 of culturing and compared to mature mucosal mast cells obtained by day20. Experiment Overall Design: The experiment was carried out on two microarrays. Array2 is a biological and technical replicate (dye-swap) of array1. In both cases, 3-3 samples were pooled, but of different origin.
2008-06-14 | E-GEOD-6192 | biostudies-arrayexpress
Project description:Experimental IgE-mediated food allergy depends on intestinal anaphylaxis driven by interleukin (IL)-9. However, the primary cellular source of IL-9 and the mechanisms underlying the susceptibility to food-induced intestinal anaphylaxis remain unclear. Herein, we have reported the identification of multifunctional IL-9-producing mucosal mast cells (MMC9s) that can secrete prodigious amounts of IL-9 and IL-13 in response to IL-33, and mast cell protease-1 (MCPt-1) in response to antigen and IgE complex crosslinking, respectively. Repeated intragastric antigen challenge induced MMC9 development that required T cells, IL-4, and STAT6 transcription factor, but not IL-9 signals. Mice ablated of MMC9 induction failed to develop intestinal mastocytosis, which resulted in decreased food allergy symptoms that could be restored by adoptively transferred MMC9s. Finally, atopic patients that developed food allergy displayed increased intestinal expression of Il9 and MC-specific transcripts. Thus, the induction of MMC9s is a pivotal step to acquire the susceptibility to IgE-mediated food allergy. dUTP mRNA-Seq profiles of indicated hematopoietic cell lineages were generated on Illumina HiSeq2500. Hematopoietic cells were isolated from Balb/C mice that developed food allergy and bone marrow-derived mast cells were generated from naïve Balb/C mice
2015-09-11 | E-GEOD-72921 | biostudies-arrayexpress
Project description:Experimental IgE-mediated food allergy depends on intestinal anaphylaxis driven by interleukin (IL)-9. However, the primary cellular source of IL-9 and the mechanisms underlying the susceptibility to food-induced intestinal anaphylaxis remain unclear. Herein, we have reported the identification of multifunctional IL-9-producing mucosal mast cells (MMC9s) that can secrete prodigious amounts of IL-9 and IL-13 in response to IL-33, and mast cell protease-1 (MCPt-1) in response to antigen and IgE complex crosslinking, respectively. Repeated intragastric antigen challenge induced MMC9 development that required T cells, IL-4, and STAT6 transcription factor, but not IL-9 signals. Mice ablated of MMC9 induction failed to develop intestinal mastocytosis, which resulted in decreased food allergy symptoms that could be restored by adoptively transferred MMC9s. Finally, atopic patients that developed food allergy displayed increased intestinal expression of Il9 and MC-specific transcripts. Thus, the induction of MMC9s is a pivotal step to acquire the susceptibility to IgE-mediated food allergy.
2015-09-11 | GSE72921 | GEO
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
Project description:Mast cells are tissue resident granulocytes which are most abundant at the interface between tissues and the external environment, such as around blood vessels, in the skin or mucosal surfaces in the lungs and gut. Pathologically they are involved in allergic reactions and anaphylaxis, however they may also play protective roles in responses to some infections, particularly to pathogenic helminths. Mast cells also express high levels of the IL-33 receptor, which like TLRs, activates Myd88 dependent signalling pathways to drive de novo cytokine production in mast cells.IL-33 is a member of the IL-1 family known to stimulate a number of immune cell types including mast cells. IL-33 is a strong activator of de novo cytokine production in mast cells without inducing degranulation, although it has also been shown to synergise with other signals to promote degranulation. Bone Marrow-Derived Mast cells (BMMCs) were cultured as described previously [27]. Briefly, bone marrow was flushed in PBS and the cells pelleted by centrifugation. Cells were cultured at 1 million cells per ml in RPMI 1640 supplemented with 10% FBS (Biosera/Labtech), 5 mM l‐Glutamine (GIBCO Life Technologies), 100 U/ml Penicillin (GIBCO Life Technologies), 100 μg/ml Streptomycin (GIBCO Life Technologies), 25 mM HEPES (Lonza), 1 mM sodium pyruvate (Lonza), 1X nonessential amino acids (Lonza), 50 μM 2‐mercaptoethanol and 30 ng/ml IL‐3 (PeproTech). Cells were passaged twice per week and used between passage 12 and 16. 4 independent BMMC cultures were either stimulated with 10 ng/ml IL-33 for 48 hours or left unstimulated, followed by single shot LC-MS analysis.
2023-03-11 | PXD033759 | Pride
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