The persisting (P) cell: histamine content, regulation by a T cell-derived factor, origin from a bone marrow precursor, and relationship to mast cells.

Schrader, John W.; Lewis, Stephen J.; Clark‐Lewis, Ian; Culvenor, Janetta G.

doi:10.1073/pnas.78.1.323

Cited by 206 publications

(94 citation statements)

References 24 publications

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“…Therefore, some morphologically identifiable mast cells in the peritoneal cavity may function as the mast cell precursors. Since peritoneal mast cells appear to float in the fluid, the proliferative potentiality of some peritoneal mast cells reminds us of the suspension culture system of mast cell-like cells that has been devised in many laboratories (41)(42)(43)(44)(45)(46). However, mitosis of peritoneal mast cells is seldom observed in intact animals (10).…”

Section: Discussionmentioning

confidence: 99%

Proliferation of peritoneal mast cells in the skin of W/Wv mice that genetically lack mast cells.

Sonoda¹,

Kanayama²,

Hara³

et al. 1984

The Journal of Experimental Medicine

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Presence of mast cell precursors in the mouse peritoneal cavity was demonstrated, and the precursors were characterized. When a cell suspension, containing mast cell precursor(s), was directly injected into the skin of genetically mast cell-deficient WBB6F1 (WB X C57BL/6)-W/Wv mice, a cluster composed of approximately 2,000 mast cells appeared at the injection site. By determining the proportion of injection sites at which the mast cell cluster appeared, the concentration of mast cell precursors can be calculated by limiting dilution analysis. The concentration in the peritoneal cavity was about five times as great as the concentration in the bone marrow. Although peritoneal mast cell precursors were shown to originate from the bone marrow, physical characterization revealed that the peritoneal precursors differed from the marrow precursors. The peritoneal precursors were less susceptible to irradiation than the marrow precursors; the former were heavier than the latter. When a 95% pure mast cell suspension was prepared from the peritoneal cells by the removal of phagocytes and the density gradient centrifugation, 1 out of 16 cells had the potentiality to make a mast cell cluster in the skin of the W/Wv mice. Moreover, when a single mast cell was identified under the phase contrast microscope and picked up with the micromanipulator, 1 out of 17 mast cells made the cluster. This indicated that some peritoneal mast cells kept extensive proliferative potentiality even after morphological differentiation. In other words, some peritoneal mast cells themselves may function as the committed precursors.

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Section: Discussionmentioning

confidence: 99%

Proliferation of peritoneal mast cells in the skin of W/Wv mice that genetically lack mast cells.

Sonoda¹,

Kanayama²,

Hara³

et al. 1984

The Journal of Experimental Medicine

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“…Mouse bone marrow-derived MCs (mBMMCs) developed with interleukin (IL) 3 (23)(24)(25) are the non-transformed cells that have been most widely used to understand at the molecular level the factors and mechanisms that regulate the proliferation, differentiation, maturation, adherence, cellular senescence, and function of mammalian MCs. For example, mBMMC cDNA libraries have been used by us to clone mouse MC protease-5, mouse MC protease-7, transmembrane tryptase, and serglycin.…”

Section: Mast Cells (Mcs)mentioning

confidence: 99%

RasGRP4, a New Mast Cell-restricted Ras Guanine Nucleotide-releasing Protein with Calcium- and Diacylglycerol-binding Motifs

Yang¹,

Li²,

Wong³

et al. 2002

Journal of Biological Chemistry

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A cDNA was isolated from interleukin 3-developed, mouse bone marrow-derived mast cells (MCs) that contained an insert (designated mRasGRP4) that had not been identified in any species at the gene, mRNA, or protein level. By using a homology-based cloning approach, the ϳ2.6-kb hRasGRP4 transcript was also isolated from the mononuclear progenitors residing in the peripheral blood of normal individuals. This transcript information was then used to locate the RasGRP4 gene in the mouse and human genomes, to deduce its exon/ intron organization, and then to identify 10 single nucleotide polymorphisms in the human gene that result in 5 amino acid differences. The >15-kb hRasGRP4 gene consists of 18 exons and resides on a region of chromosome 19q13.1 that had not been sequenced by the Human Genome Project. Human and mouse MCs and their progenitors selectively express RasGRP4, and this new intracellular protein contains all of the domains present in the RasGRP family of guanine nucleotide exchange factors even though it is <50% identical to its closest homolog. Recombinant RasGRP4 can activate H-Ras in a cation-dependent manner. Transfection experiments also suggest that RasGRP4 is a diacylglycerol/phorbol ester receptor. Transcript analysis of an asthma patient, a mastocytosis patient, and the HMC-1 cell line derived from a MC leukemia patient revealed the presence of substantial amounts of non-functional forms of hRas-GRP4 due to an inability to remove intron 5 in the precursor transcript. Because only abnormal forms of hRas-GRP4 were identified in the HMC-1 cell line, this immature MC progenitor was used to address the function of RasGRP4 in MCs. HMC-1 leukemia cells differentiated and underwent granule maturation when induced to express a normal form of RasGRP4. Thus, RasGRP4 plays an important role in the final stages of MC development.

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“…It supports the growth and/or differentiation of multipotent precursor cells belonging to both the myeloid and lymphoid lineages as well as more differentiated progenitor cells belonging to the myeloid lineage (2,(11)(12)(13)(14)(15). IL-3 has also been associated with multiple activities and has been termed burstpromoting activity (16), mast cell growth factor (17,18), P cell stimulating factor (19,20), and histamine-producing cell-stimulating factor (21) by various investigators.…”

mentioning

confidence: 99%

Activation and growth of colony-stimulating factor-dependent cell lines is cell cycle stage dependent.

London

McKearn

1987

The Journal of Experimental Medicine

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Hematopoietic cell development is regulated by a series of growth factors that are progressively restricted in their biological activity. IL-3 is a multi-lineage growth factor that supports the growth and differentiation of progenitor cells belonging to multiple lineages. However, the mechanism by which IL-3 induces proliferation and differentiation of these cells is not completely understood. In this report, we have used two IL-3-dependent cell lines, FDC-P1 (a myeloid progenitor) and F15.12 (a lymphoid progenitor) to investigate IL-3-mediated growth and differentiation. When either FDC-P1 or FL5.12 cells are deprived of IL-3, greater than 90% of all cells accumulate in the G0 phase of the cell cycle. Upon readdition of IL-3, the cells will reenter the active phases of the cell cycle. Therefore, IL-3 can act as both a competence (G0----G1) factor, and a progression (G1----M) factor for hematopoietic precursor clones. FDC-P1 cells can also proliferate in response to granulocyte/macrophage colony-stimulating factor (G/M-CSF) and IL-4 (B cell stimulatory factor 1 [BSF-1]). However, resting (G0) FDC-P1 cells have lost their ability to grow in response to both G/M-CSF and IL-4, even though both factors can induce a G0----G1 transition. Therefore, G/M-CSF or IL-4 behave as progression factors among certain IL-3-responsive clones, and in those cases only in defined points in the cell cycle. Both IL-4 and G/M-CSF can maintain long-term growth of FDC-P1 cells. Upon removal of factor for 24 h, these clones accumulate in the G1 phase of the cell cycle and do not appear to enter G0 even after 36 h of factor deprivation. Therefore, cells maintained in G/M-CSF or IL-4 have altered growth requirements compared with the IL-3-dependent lines from which they were derived. The ability of various hematopoietic growth factors to regulate cell cycle progression in IL-3-dependent cell lines is dependent not only upon the lineage from which these cells were derived, but also the phase of the cell cycle in which those cells reside. The consequences of these interactions dictate the manner by which various clones will respond to CSFs and whether the cells will grow and/or differentiate.

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The persisting (P) cell: histamine content, regulation by a T cell-derived factor, origin from a bone marrow precursor, and relationship to mast cells.

Cited by 206 publications

References 24 publications

Proliferation of peritoneal mast cells in the skin of W/Wv mice that genetically lack mast cells.

Proliferation of peritoneal mast cells in the skin of W/Wv mice that genetically lack mast cells.

RasGRP4, a New Mast Cell-restricted Ras Guanine Nucleotide-releasing Protein with Calcium- and Diacylglycerol-binding Motifs

Activation and growth of colony-stimulating factor-dependent cell lines is cell cycle stage dependent.

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