Next-generation sequencing facilitates quantitative analysis of wild-type peritoneal murine mast cells (PMCs) and their comparison to PMC lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE227065 | GEO | 2023/03/14
REPOSITORIES: GEO
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Project description:We report the single-cell transcriptional profiling of sea urchin primary mesenchyme cells isolated from embryos treated with DMSO or with 5-lox activating protein (FLAP) inhibitor MK-886. We find that inhibition of LOX activity with MK-886 prior to PMC isolation induces shifts in gene expression within the PMC population. We further demonstrate that control PMCs cluster into four transcriptionally-defined subsets, and MK-886-treated PMCs cluster into five distinct subsets. These data highlight novel transcriptional paradigms in the diversification of PMCs, and the requirement of ectodermal LOX activity for proper PMC transcriptional diversification.
2022-06-01 | GSE164240 | GEO
Project description:Local administration of IFN-α-producing proliferating myeloid cells (IFN-α-iPSC-pMCs) inhibited the tumor growth not only at the treatment site (right) but also at the distant site (left). We identified genes with log fold expression change ≥ 1 or ≤ −1 in untreated versus IFN-α-iPSC-pMC-treated tumors and iPSC-pMC-treated versus IFN-α-iPSC-pMC-treated tumors for treatment or distant site, respectively. Of the overlapping genes differentially expressed in IFN-α-iPSC-pMC-treated mice, 301/671 distant site and 460/928 treated site genes were ISGs, of which 95.3% and 94.7%, respectively, were type I IFN-related. By gene ontology, the up-regulated ISG signatures were enriched for “T cell-mediated immune responses”, “cytolysis”, and “migration of immune cells” associated genes. Collectively, Local administration of IFN-α-iPSC-pMCs alters the tumor microenvironment and propagates molecular signature associated with type I IFN.
2019-02-13 | GSE126279 | GEO
Project description:We are interested in comparing expression patterns of hematopoletic stem cells, mast cell precursors and mature mast cells. Our group recently reported that murine mast cells express CD34, Sca-1 and c-kit. Microarray analysis may uncover other novel surface antigens useful in separating mast cells from stem cells. Experiment Overall Design: this experiment include 2 samples and 12 replicates
2008-06-12 | E-GEOD-3776 | biostudies-arrayexpress
Project description:We are interested in comparing expression patterns of hematopoletic stem cells, mast cell precursors and mature mast cells. Our group recently reported that murine mast cells express CD34, Sca-1 and c-kit. Microarray analysis may uncover other novel surface antigens useful in separating mast cells from stem cells. Keywords: other
2005-12-09 | GSE3776 | GEO
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
Project description:We previously established a method to generate myeloid lineage cells with proliferation capacity from induced pluripotent stem cells (iPSCs) (Zhang R. Cancer Immunol Res. 3: 668, 2015). In this study, we generated the IFN-α-producing cells by genetic engineering of mouse iPSC-derived myeloid cells (iPSC-pMCs). Gene expression profiling of IFN-α-producing iPSC-pMCs (IFN-α-iPSC-pMCs) revealed a distinct interferon-stimulated gene (ISG) signature: of 613 differentially expressed genes (versus iPSC-pMC), 345 genes were ISGs of which > 70 % were type I IFN-related. Gene ontology analysis showed that the up-regulated gene signature was enriched for transcripts associate with immune responses, cellular responses to type I IFN, and defense responses to virus.
2019-02-13 | GSE126277 | GEO
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: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.
2011-01-25 | GSE26783 | GEO
Project description:Investigations of teriparatide (rPTH) as a potential treatment for critical defects have demonstrated the predicted anabolic effects on bone formation, and significant non-anabolic effects on healing via undefined mechanisms. Specifically, studies in murine models of structural allograft healing demonstrated that rPTH treatment increased angiogenesis (vessels <30μm), and decreased arteriogenesis (>30 μm) and mast cell numbers, which lead to decreased fibrosis and accelerated healing. To better understand these non-anabolic effects, we interrogated osteogenesis, vasculogenesis and mast cell accumulation in mice randomized to placebo (saline), rPTH (20µg/kg/2days), or the mast cell inhibitor sodium cromolyn (SC) (24µg/kg/2days), via longitudinal micro-CT and multiphoton laser scanning microscopy (MPLSM), in a critical calvaria defect model. Micro-CT demonstrated that SC significantly increased defect window closure and new bone volume versus placebo (p<0.05), although these effects were not as great as rPTH. Interestingly, both rPTH and SC has similar inhibitory effects on arteriogenesis versus placebo (p<0.05) without affecting total vascular volume. MPLSM time course studies in untreated mice revealed that large numbers of mast cells were detected 1 day post-op (43 +/- 17), peaked at 6 days (76 +/- 6), and were still present in the critical defect at the end of the experiment on day 30 (20 +/- 12). In contrast, angiogenesis was not observed until day 4, and functional vessels were first observed on 6 days, demonstrating that mast cell accumulation precedes vasculogenesis. To confirm a direct role of mast cells on osteogenesis and vasculogenesis, we demonstrated that specific diphtheria toxin-α deletion in Mcpt5-Cre-iDTR mice results in similar affects as SC treatment in WT mice. Collectively, these findings demonstrate that mast cells inhibit bone defect healing by stimulating arteriogenesis associated with fibrotic scaring, and that an efficacious non-anabolic effect of rPTH therapy on bone repair is suppression of arteriogenesis and fibrosis secondary to mast cell inhibition.And then, we need to figure out how rPTH works on mast cells. So we used the co-culture of osteoblast and mast cells, and perform RNAseq, by which we aim to screen out the factors in mast cells that are potential mediators for rPTH effects in bone formation, blood vessel formation, and fibrosis formation.
2017-08-21 | GSE98510 | GEO
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 human and mouse mast cells by quantitative mass spectrometry. We identified a mast cell-specific protein signature that was conserved from mouse to man. Compared to a comprehensive set of other immune cell lineages, proteome analysis identified a unique and distant mast cell cluster. The mast cell signature included proteins governing granule biosynthesis and secretion, as well as proteoglycan- and neurotransmitter metabolism. Proteome conservation across species suggests evolutionary maintenance of mast cell functions.
2020-02-12 | PXD014978 | Pride