Microarray analysis of Bone marrow derived mast cells (BMMCs) from C57BL/6 and ACKR2-/- mice
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ABSTRACT:
PROVIDER: PRJNA414031 | ENA |
REPOSITORIES: ENA
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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:Gene expression profile of Pafah2-deficient bone marrow derived mast cells (BMMCs) treated with w3 epoxides or GW9662
2017-02-07 | GSE94527 | 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:Purpose:The purpose of this study is to detect activated or silenced genes during Tet2-deficient bone marrow derived mast cell (BMMC) and the control cells. Gene expression differences between two samples could be found using transcriptome profiling (RNA-seq) analysis. Methods:Mouse BMMCs were generated from bone marrow cells in RPMI-1640 medium with recombinant mouse IL-3 and SCF. BMMCs were stained to confirm the surface expression of FcɛRI and c-Kit. Cells with purity >97.5% were used for subsequent experiments. BMMCs RNA profiles were generated by deep sequencing,using Illumina. Results: We mapped about 10 million sequence reads per sample to the mouse genome, identified hundreds of genes with significant mRNA variation between Tet2-deficient BMMC and the control cells.
2018-01-25 | GSE100560 | GEO
Project description:Bone marrow-derived mast cells were derived from three different female C57Bl/6 mice of similar age. Cells were transduced with pAPM lentiviruses either overexpressing microRNA-221 or a non functional microRNA-221 mutant, termed miR-221m, where four point-mutations were introduced in the seed sequence of miR-221. The samples overexpressing miR-221m were used as references for the corresponding miR-221 overexpressing BMMCs from the same mouse (mouse matched reference). The experiment was performed in order to gain more insights about the molecular mechanisms underlying miR-221 effects in mast cells.
2011-11-23 | GSE24462 | GEO
Project description:Purpose: To transcriptome widely reveal 5-mC regulation by Tet2, we performed bisulfite-sequencing of mRNAs from Tet2-deficient BMMCs and the control cells.Methods: Mouse BMMCs were generated from bone marrow cells in RPMI-1640 medium with recombinant mouse IL-3 and SCF. BMMCs were stained to confirm the surface expression of FcɛRI and c-Kit. Cells with purity >97.5% were used for RNA isolation. Results: We carried out an unbiased global analysis of m5C in poly(A)RNA of mouse bone marrow derived mast cells (BMMCs).We show that there were indeed much more mCs in Tet2-deficient group compared with the control, more than half of which located in genic region. Furthermore, we observed that although much less mCs distributed in the three elements of exon regions, more mCs located in 3`-UTR for Tet2-deficient group compared with the control.
2018-01-25 | GSE100719 | GEO
Project description:Bone marrow-derived mast cells were derived from three different female C57Bl/6 mice of similar age. Cells were transduced with pAPM lentiviruses either overexpressing microRNA-221 or a non functional microRNA-221 mutant, termed miR-221m, where four point-mutations were introduced in the seed sequence of miR-221. The samples overexpressing miR-221m were used as references for the corresponding miR-221 overexpressing BMMCs from the same mouse (mouse matched reference). The experiment was performed in order to gain more insights about the molecular mechanisms underlying miR-221 effects in mast cells. Two-condition experiment, BMMC overexpressing miR-221 vs BMMC overexpressing miR-221m. Biological replicates: 3 replicates overexpressing miR-221, 3 control replicates overexpressing miR-221m.
2011-11-23 | E-GEOD-24462 | biostudies-arrayexpress
Project description:Allergy is one of the least understood immunological response partly due to the diversity of allergens and the complexity of immune response against them. In allergic responses, mast cells are key players with their ability to rapidly degranulate and also generate de novo lipids and transcripts. Although the molecular details of degranulation in mast cell were studied in allergic inflammation, the transcriptional response involving chromatin remodeling, enhancer dynamics and long non-coding RNA (lncRNA) expression are largely unexplored. Here, using mouse bone marrow derived mast cells (BMMCs), we characterized the steady state, immunoglobulin E (IgE) and antigen (Ag) mediated epigenetic changes in mast cell chromatin and described the enhancer, super-enhancer and mRNA, lncRNA catalogue in these cells.
2019-12-01 | GSE75526 | GEO
Project description:Allergy is one of the least understood immunological response partly due to the diversity of allergens and the complexity of immune response against them. In allergic responses, mast cells are key players with their ability to rapidly degranulate and also generate de novo lipids and transcripts. Although the molecular details of degranulation in mast cell were studied in allergic inflammation, the transcriptional response involving chromatin remodeling, enhancer dynamics and long non-coding RNA (lncRNA) expression are largely unexplored. Here, using mouse bone marrow derived mast cells (BMMCs), we characterized the steady state, immunoglobulin E (IgE) and antigen (Ag) mediated epigenetic changes in mast cell chromatin and described the enhancer, super-enhancer and mRNA, lncRNA catalogue in these cells.
2019-12-01 | GSE75525 | GEO
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