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Adult Connective Tissue-Resident Mast Cells Originate from Late Erythro-Myeloid Progenitors [development]

ABSTRACT: Purpose: The purpose is to systemically identify RNA expression changes along mast cell development during embryogenesis. Methods: We profiled RNA-seq in early EMPs and their progeny. Results: Fetal MCPs acquire the mast cell-specific gene signature from E11.5 and complete their maturation in peripheral tissues.

ORGANISM(S): Mus musculus

PROVIDER: GSE119017 | GEO | 2018/10/15

REPOSITORIES: GEO

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Adult Connective Tissue-Resident Mast Cells Originate from Late Erythro-Myeloid Progenitors [origins]

Project description:Purpose: The purpose is to systemically identify RNA expression between skin mast cells with distinct origins. Methods: We profiled RNA-seq in skin mast cells with distinct origins. Results: Early, late EMP and fetal HSC-derived skin mast cells display distinct transcriptome profiles.

2018-10-05 | GSE119016 | GEO

Adult Connective Tissue-Resident Mast Cells Originate from Late Erythro-Myeloid Progenitors

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-10-09 | GSE119018 | GEO

Adult Connective Tissue-Resident Mast Cells Originate from Late Erythro-Myeloid Progenitors

Project description:Adult Connective Tissue-Resident Mast Cells Originate from Late Erythro-Myeloid Progenitors

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Adult Connective Tissue-Resident Mast Cells Originate from Late Erythro-Myeloid Progenitors [origins]

Project description:Adult Connective Tissue-Resident Mast Cells Originate from Late Erythro-Myeloid Progenitors [origins]

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Adult Connective Tissue-Resident Mast Cells Originate from Late Erythro-Myeloid Progenitors [development]

Project description:Adult Connective Tissue-Resident Mast Cells Originate from Late Erythro-Myeloid Progenitors [development]

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Human connective tissue mast cell proteome

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

Mouse connective tissue mast cell proteome

2020-02-12 | PXD015040 | Pride

Class IA PI3Kinase regulatory subunit p85α regulates mast cell growth and survival related genes

Project description:Stem cell factor (SCF) mediated KIT receptor activation plays a pivotal role in mast cell growth, maturation and survival. However, the signaling events downstream from KIT are poorly understood. Mast cells express multiple regulatory subunits of class 1A PI3Kinase (PI3K) including p85α, p85β, p50α, and p55α. While it is known that PI3K plays an essential role in mast cells; the precise mechanism by which these regulatory subunits impact specific mast cell functions including growth, survival and cycling are not known. We show that loss of p85α impairs the growth, survival and cycling of mast cell progenitors (MCp). To delineate the molecular mechanism (s) by which p85α regulates mast cell growth, survival and cycling, we performed microarray analyses to compare the gene expression profile of MCps derived from WT and p85α-deficient mice in response to SCF stimulation. We identified 151 unique genes exhibiting altered expression in p85α-deficient cells in response to SCF stimulation compared to WT cells. Functional categorization based on DAVID bioinformatics tool and Ingenuity Pathway Analysis (IPA) software relates the altered genes due to lack of p85α to transcription, cell cycle, cell survival, cell adhesion, cell differentiation, and signal transduction. Our results suggest that p85α is involved in mast cell development through regulation of expression of growth, survival and cell cycle related genes. Two-condition experiment, wildtype vs. p85α-deficient mast cell progenitors stimulated with SCF. Biological replicates: 3 wildtype replicates, 3 p85α-deficient replicates.

2011-09-27 | E-GEOD-32410 | biostudies-arrayexpress

Class IA PI3Kinase regulatory subunit p85α regulates mast cell growth and survival related genes

2011-09-28 | GSE32410 | GEO

Erythro-myeloid progenitors contribute endothelial cells to developing blood vessels

Project description:The earliest blood vessels in the mammalian embryo are formed when endothelial cells (ECs) differentiate from angioblasts and coalesce into tubular networks. Thereafter, the en-dothelium is thought to expand solely by proliferation of pre-existing ECs. Here we show that the earliest precursors of erythrocytes, megakaryocytes and macrophages, the yolk sac-derived erythro-myeloid progenitors (EMPs), provide a complementary source of ECs that are recruited into pre-existing vasculature. Whereas a first wave of yolk sac-resident EMPs contributes ECs to the yolk sac endothelium, a second wave of EMPs colonises the embryo and contributes ECs to intraembryonic endothelium in multiple organs, where they persist into adulthood. By demonstrating that EMPs constitute a hitherto unrecognised source of ECs, we reveal that embryonic blood vascular endothelium expands in a dual mechanism that involves both the proliferation of pre-existing ECs and the incorporation of ECs derived from hematopoietic precursors.

2018-08-02 | GSE117978 | GEO

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