Influence of pseudoallergy-positive compounds on the transcription of HMC-1 mast cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE329896 | GEO | 2026/09/16
REPOSITORIES: GEO
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Project description:Four typical pseudoallergy-positive compounds, including C48/80, PAMP-12, Substance P and (R)-ZINC-3573, were selected as stimulants to induce cell degranulation. This study aims to systematically investigate the transcriptional expression alterations in mast cells and analyze the transcriptomic characteristics associated with pseudoallergy.
2026-09-16 | GSE330505 | GEO
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
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
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:Influence of pseudoallergy-positive compounds on the transcription of HMC-1 mast cells
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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:Steroid hormones are well known regulators of mast cell function, but whether mast cells themselves produce steroids de novo and influences their effector function has remained unknown. Here, we show that mast cells constitutively express the steroidogenic enzyme Cyp11a1 and produce pregnenolone. Cyp11a1 expression was detected across tissue-resident mast cells from multiple organs, was conserved in human mast cells, and was enhanced by IL-3 signalling and after activation. We identified Cyp11a1 as a Gata2-dependent, super-enhancer-associated mast cell gene, placing steroidogenesis within the core mast cell transcriptional programme. Loss of Cyp11a1 altered transcriptomic and proteomic programmes in mast cells, with effects on pathways linked to cell growth, immune signalling, and effector function. Functionally, Cyp11a1-deficient mast cells showed increased degranulation in response to both IgE-dependent and IgE-independent stimulation. In vivo, loss of Cyp11a1 reduced mast cell abundance in several tissues but exacerbated passive cutaneous anaphylaxis. These findings identify cell-intrinsic steroidogenesis as a regulatory pathway that restrains mast cell activation and anaphylactic responses
2026-09-04 | PXD079414 | Pride
Project description:Steroid hormones are well known regulators of mast cell function, but whether mast cells themselves produce steroids de novo and influences their effector function has remained unknown. Here, we show that mast cells constitutively express the steroidogenic enzyme Cyp11a1 and produce pregnenolone. Cyp11a1 expression was detected across tissue-resident mast cells from multiple organs, was conserved in human mast cells, and was enhanced by IL-3 signalling and after activation. We identified Cyp11a1 as a Gata2-dependent, super-enhancer-associated mast cell gene, placing steroidogenesis within the core mast cell transcriptional programme. Loss of Cyp11a1 altered transcriptomic and proteomic programmes in mast cells, with effects on pathways linked to cell growth, immune signalling, and effector function. Functionally, Cyp11a1-deficient mast cells showed increased degranulation in response to both IgE-dependent and IgE-independent stimulation. In vivo, loss of Cyp11a1 reduced mast cell abundance in several tissues but exacerbated passive cutaneous anaphylaxis. These findings identify cell-intrinsic steroidogenesis as a regulatory pathway that restrains mast cell activation and anaphylactic responses
2026-09-04 | PXD079140 | Pride
Project description:Mast cells are hematopoietic cells that reside preferentially in tissues exposed to internal and external environments. Mast cells sense immunological, inflammatory and environmental stimuli, and can be activated to release granules and generate inflammatory mediators. Mast cell-derived products confer protection against snake venoms and some parasite infections. Aberrant activation of mast cells is a major contributor to human pathology, including allergy, asthma and adverse drug reactions. Their strict tissue location has largely impeded the isolation of large numbers of primary mast cell for further analysis. To better understand the biology of mast cells, we analyzed the proteome of primary mouse mast cells by quantitative mass spectrometry
2020-02-12 | PXD015040 | 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