Differential roles of GATA‐1 and GATA‐2 in growth and differentiation of mast cells

Harigae, Hideo; Takahashi, Satoru; Suwabe, Naruyoshi; Ohtsu, Hiroshi; Gu, Lin; Yang, Zhouying; Tsai, Fong Ying; Kitamura, Yukihiko; Engel, James Douglas; Yamamoto, Masayuki

doi:10.1046/j.1365-2443.1998.00166.x

Cited by 83 publications

(89 citation statements)

References 49 publications

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“…Mast cells arise from the common myeloid progenitor (CMP) in bone marrow (37,38). Several transcription factors and cytokines are involved in differentiation of these cells including GATA-1, GATA-2, PU.1, MITF, IL-3 and stem cell factor (39)(40)(41). Mast cells express specific pattern of Notch family members, low level of Notch-1, high level of Notch-2 and detectable level of Notch-3 (42).…”

Section: Notch and Myeloid Cell Differentiationmentioning

confidence: 99%

“…Recently, Taghon et al have found that overexpression of GATA-3 acts as antagonist of Notch, blocking pro-T cell survival. In the absence of Notch signaling, GATA-3 overexpression differentiates lymphoid progenitors from fetal liver and T precursors to mast cell through upregulation of GATA-1 and GATA-2 (45), the genes that are essential for mast cell development (41,46).…”

Section: Notch and Myeloid Cell Differentiationmentioning

confidence: 99%

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Notch signaling in differentiation and function of dendritic cells

Cheng

Gabrilovich

2007

Immunol Res

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Hematopoietic stem cells give rise to multiple lineages of cells. This process is governed by a tightly controlled signaling network regulated by cytokines and a direct cell-cell. Notch signaling represents one of the major pathways activated during direct interaction between hematopoietic progenitor cells and bone marrow stroma. A critical role of Notch signaling in differentiation of T and B lymphocytes has now been established. Until recently, the role of Notch signaling in the development of myeloid cells and particular dendritic cells remained unclear. In this review we discuss recent exciting findings that shed light on the critical role of Notch in differentiation and the function of dendritic cells and its impact on immune responses.

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Section: Notch and Myeloid Cell Differentiationmentioning

confidence: 99%

Section: Notch and Myeloid Cell Differentiationmentioning

confidence: 99%

Notch signaling in differentiation and function of dendritic cells

Cheng

Gabrilovich

2007

Immunol Res

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“…Mast cells express high levels of GATA-1 and GATA-2. The role of GATA in chymase gene transcription has not been explored, 43,44 but has previously been shown in P815 mast cells. 45 Various studies suggested that AP-1, which is a dimeric complex of a Jun family protein and a Fos family protein, may functionally interact with GATA proteins.…”

Section: Discussionmentioning

confidence: 99%

Homocysteine-induced oxidative stress upregulates chymase in mouse mastocytoma cells

et al. 2009

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Reactive oxygen species (ROS) such as hydrogen peroxide (H 2 O 2 ), O À 2 and OH participate in the pathogenesis of ischemia/ reperfusion injury, inflammation and atherosclerosis. Our previous studies have suggested that increased angiotensin II (Ang II)-forming chymase may be involved in the development of atherosclerosis. However, the regulatory mechanism of chymase expression has not yet been clarified. In this study, we tested whether oxidative stress upregulates mouse mast cell proteinase chymase, mouse mast cell proteinase (MMCP)-5 or MMCP-4. We also examined the expression and activity of these proteins after treatment. Cultured mouse mastocytoma cells (MMC) displaying chymase-dependent Ang II-forming activity were treated with H 2 O 2 and several aminothiols with or without anti-oxidants. The levels of MMCP-5 and MMCP-4 expression were determined by quantitative RT-PCR; the level of chymase-dependent Ang II-forming activity was measured by high performance liquid chromatography using Ang I as a substrate. Treatment of MMC with homocysteine (0.1-3 mmol l -1 ) significantly increased MMCP-5 and MMCP-4 expression, as well as Ang II-forming activity. These effects were significantly inhibited by the addition of catalase and further suppressed by the combination of catalase and superoxide dismutase. Incubation with hydrogen peroxide alone caused a significant increase in Ang II-forming activity, which was completely suppressed by co-treatment with catalase. Furthermore, MMCP-5 and MMCP-4 expression levels were drastically suppressed and chymase induction by homocysteine was diminished under the GATA-inhibited condition. Homocysteine increased mast cell chymase expression and activity through the mechanism of oxidative stress. Our results suggest that there is a biochemical link between oxidative stress and the local Ang IIforming system.

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“…In addition, committed mast cell progenitors from these mice cannot be detected in the marrow, but mast cells can be derived from the megakaryocyte-erythroid progenitor population (34). A deletion of the proximal erythroid promoter of GATA-1 (GATA-1 "enfeebled") also results in reduced GATA-1 expression(35); these mice display reduction in mature mast cells in the skin (36). Mast cell target genes have been identified for GATA-1, including the alpha and beta chains of FcεRI(37;38), carboxypeptidase A(39), interleukin-4(40), and interleukin-13 (41).…”

Section: Gata-1 and Gata-2mentioning

confidence: 99%

“…These mutant mice have lower GATA-1 levels and more severe anemia and thrombocytopenia (81). In addition, there is a reduction in the mature mast cells that normally populate the skin (82). A specific deletion of a GATA palindromic binding site region upstream of the neomycin insertion site and the IE exon resulted in a selective defect in eosinophil development (83).…”

Section: Regulation Of the Gata-1 Locus In Mast Cellsmentioning

confidence: 99%

Mast cell transcriptional networks

Takemoto

Lee

Jegga

et al. 2008

Blood Cells, Molecules, and Diseases

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Unregulated activation of mast cells can contribute to the pathogenesis of inflammatory and allergic diseases, including asthma, rheumatoid arthritis, inflammatory bowel disease, and multiple sclerosis (1;2). Absence of mast cells in animal models can lead to impairment in the innate immune response to parasites and bacterial infections (3)(4)(5). Aberrant clonal accumulation and proliferation of mast cells can result in a variety of diseases ranging from benign cutaneous mastocytosis to systemic mastocytosis or mast cell leukemia(6). Understanding mast cell differentiation provides important insights into mechanisms of lineage selection during hematopoiesis and can provide targets for new drug development to treat mast cell disorders,. In this review, we discuss controversies related to development, sites of origin,, and the transcriptional program of mast cells. KeywordsMast cells; transcription factors; GATA; PU.1; Mitf Origins of Mast CellsLike other granulocytes (neutrophils, eosinophils and basophils), mast cells are derived from hematopoietic stem cells in the marrow; however, they are unique with regard to the tissue compartments in which they traffic and reside. The gastrointestinal mucosa is the major compartment occupied by committed mast cell precursors in the mouse (7). Trafficking to these compartments is dependent on the expression of the alpha4 beta7 integrin and the chemokine receptor CXCR2.(8;9) Mast cell progenitors migrate to the connective tissue of the skin, lung, and the mucosa of other gastrointestinal tissues where they mature under the influence local Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Transplantation studies in mice indicate that mast cells are derived from hematopoietic stem cells of marrow (or spleen)(10;11). Studies using prospectively identified hematopoietic precursors have reported different precursor cells that give rise to the committed mast cell progenitor One study found that the committed mast cell progenitor (MCP) arose from an early multipotential progenitor (MPP) that is distinct from the common myeloid progenitor (12). However, using a similar strategy to prospectively isolate hematopoietic precursors from mouse marrow, another study found that the MCP was derived from either the common myeloid progenitor or the granulocyte-monocyte progenitor(13) (Figure 1). Plasticity may permit other committed progenitor cell populations to be "reprogrammed" into the mast cell lineage by altering the expression of selected transcription factors. Isolated common lymphoid precursors that are retrovirally-tranduced with the tr...

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Differential roles of GATA‐1 and GATA‐2 in growth and differentiation of mast cells

Cited by 83 publications

References 49 publications

Notch signaling in differentiation and function of dendritic cells

Notch signaling in differentiation and function of dendritic cells

Homocysteine-induced oxidative stress upregulates chymase in mouse mastocytoma cells

Mast cell transcriptional networks

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