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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mast cells produce a variety of enzymes and vasoactive, chemotactic, and bronchoconstrictor substances in response to nonimmunologic as well as immunologic stimuli. These mast cell-derived mediators may act on airway smooth muscle, submucosal glands, epithelial cells, circulating blood cells, vascular cells, and other cell types. The secretory profile of a mast cell appears to depend on the specific stimulus applied. In addition, different populations of mast cells exist, and distinct enzymatic pathways may predominate in different cell types. The effect of mast cell-derived mediators on the various target cells may be direct or indirect. For example, mediators released by immunologic challenge of sensitized lung fragments or by nonimmunologic challenge of canine mastocytoma cells stimulate the transport of ions and water across the tracheal epithelium. This effect, however, is indirect, is blocked by indomethacin, and therefore appears to be dependent upon an intact cyclooxygenase pathway in the tracheal epithelium. Canine mastocytoma cells resemble normal mast cells in dog lung and skin, and can be propagated to provide a continuous source of large numbers of pure, identical mast cells for biochemical and physiologic studies. Studies of these cells and their inflammatory mediators will increase our understanding of the complex series of cell-to-cell interactions which are responsible for the pathophysiologic manifestations of obstructive lung disease.
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PMID:Mast cell-derived mediators and their role in cell-to-cell interactions in the lung. 356 13

Histochemical and electron-microscopic studies of skin biopsy specimens from 65 patients with mastocytosis have enabled the authors to classify the various mastocytoses (on the basis of infiltrate topography and structural features of mast cells) into macular, pustular, and nodular varieties of cutaneous mastocytosis (urticaria pigmentosa) and mastocytoma. No differences in mast cell structure were detected between cutaneous and systemic mastocytoses. Electron microscopically, mast cells in both appeared normal, with a predominance of granules having a fine-grained or homogeneous matrix and a small number of lamellar structures. In mastocytomas, on the other hand, ultrastructural changes and considerable degranulation were observed in the mast cells.
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PMID:[Morphology of mastocytosis]. 366 56

Normal murine peritoneal mast cells were fused to serum-deprived, non-proliferating cells of a cultured subline (41-SB-4) of the P-815 murine mastocytoma. Upon reincubation in medium containing 10% horse serum for 48 h, mono- and binuclear 41-SB-4 cells reentered S phase of the cell cycle, while mast cell X 41-SB-4 heterokaryons as well as mono- and binuclear mast cells remained in proliferative quiescence, indicating dominant expression of the quiescent state of mast cells. The quiescent state of normal mast cells thus resembles that of cold-sensitive (cs) mutant cells (21-F) of the undifferentiated P-815 mastocytoma: at the non-permissive temperature of 33 degrees C, the 21-F cells were found to enter a state of quiescence which is characterized by its dominant expression in heterokaryons and by morphological differentiation with the formation of metachromatically staining granules similar to those of mast cells. This suggests that the cellular control mechanisms involved in entry into proliferative quiescence and in morphological differentiation of cs 21-F cells may be analogous to those of normal mast cells and/or their precursors.
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PMID:Proliferative quiescence of normal mast cells resembles that of cold-sensitive mutant mastocytoma cells. Dominant expression of the quiescent state in heterokaryons. 392 78

Systemic mastocytosis, with its diffuse infiltration of mast cells into various organs, has resulted in intestinal malabsorption and bleeding diatheses. The pathophysiology underlying these phenomena is unclear, but may be related to the release of histamine and heparin containing mast cell granules. A patient with systemic mastocytosis had malabsorption and developed massive bleeding after percutaneous liver biopsy. Histologic involvement of skin, duodenum, rectum, liver, and bone marrow was documented. Mastocytosis should be considered in the differential diagnosis of malabsorption.
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PMID:Bleeding after liver biopsy in a patient with systemic mastocytosis and malabsorption. 404 81

A neoplastic mast cell tumor was grown in mice which had been raised since birth on a diet enriched with eicosapentaenoic acid. Intact harvested mastocytoma cells were stimulated with calcium ionophore A23187 to produce lipoxygenase products from the polyunsaturated fatty acids liberated from the cellular membranes. Leukotriene B4, B5, C4, and C5 were isolated and characterized by HPLC retention time, ultraviolet absorption spectrometry and mass spectrometry. The arachidonic acid content of the mast cell tumor lipids was altered from 9.2 to 3.9 mole % while eicosapentaenoic acid increased from 0.5 to 4.5 mole % in response to the fish oil-supplemented diet. The relative amounts of arachidonic and eicosapentaenoic acids (3.9 and 4.5 mole % respectively) were associated with similar amounts of LTB4 and LTB5 synthesized by the cells. These results suggest that the epoxide leukotriene (LIA) derivative can be made efficiently from either arachidonic or eicosapentaenoic acids when both are present in cellular lipids. In contrast, the ratio of LTC4 to LTC5 (10 to 1) indicates that the reaction of LTA with glutathione may be critically dependent upon the structure of the unsaturated fatty acid with the ratio of LTC4/LTB4 (2.0) more than 10 times greater than that (0.16) for LTC5/LTB5.
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PMID:Tetraene and pentaene leukotrienes: selective production from murine mastocytoma cells after dietary manipulation. 611 40

Bone marrow-derived mast cells, differentiated in vitro, demonstrate surface IgE, receptors and contain histamine in metachromatic granules, which are composed of chondroitin sulfate E proteoglycan rather than heparin proteoglycan. Activation of this subclass of mast cells with calcium ionophore A23187 resulted in generation of immunoreactive C-6-sulfidopeptide leukotriene in a dose- and time-dependent fashion. Isolation of immunoreactive C-6-sulfldopeptide leukotriene by reverse-phase high-performance liquid chromatography (RP-HPLC) revealed a retention time and a specific biologic activity identical to those of synthetic leukotriene C4 (LTC4). Neither radiolabeled nor immunoreactive conversion products of [3H]LTC4/LTC4 were recognized during RP-HPLC resolution of the supernatants. The failure of fresh bone marrow cultures to generate C-6-sulfidopeptide leukotriene in response to ionophore indicates that leukotriene generation is dependent upon cellular differentiation into a mast cell population. The amount of LTC4 generated during optimal ionophore stimulation, 90.9 +/- 7.5 ng per 10(6) cells, contrasts with the relatively low amounts of C-6-sulfidopeptide leukotriene generated by the conventional heparin-containing rat mast cells or mouse mastocytoma cells.
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PMID:Generation of leukotriene C4 from a subclass of mast cells differentiated in vitro from mouse bone marrow. 612 76

The specific activities of pyruvate kinase and phosphofructokinase but not lactate dehydrogenase increase as P-815 mastocytoma cells approach the stationary phase. During this growth period, the rates of uptake of labelled precursors into DNA, RNA and total protein decreases. On the other hand, the pyruvate kinase protein level changes in parallel with activity. Although the K-isozyme is the primary form of pyruvate kinase expressed, some M-type subunit is also present and both forms undergo an increase in specific activity. In addition, pyruvate kinase expression is also elevated by adding cAMP analogues with theophylline, butyrate or conditioned media. This increased level of expression is hypothesized to be a secondary event associated with a differentiation-like-induced expression of the mast cell phenotype.
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PMID:Regulation of pyruvate kinase expression and growth in mastocytoma cells. I. Initial observations. 619 20

Isolated dog mastocytoma cells sensitized with dog anti-ragweed IgE and challenged with ragweed antigen generate the C-6 peptide leukotriene (LT) constituents of the slow-reacting substance of anaphylaxis (SRS-A), LTC4 and LTD4, and the potent leukocyte chemotactic factor, LTB4, as well as 15-hydroxyeicosatetraenoic acid (15-HETE), 12-HETE, and 5-HETE. Antigen challenge evoked a mean maximum production of LTC4, LTD4, and LTB4, respectively, of 16.3 ng, 4.6 ng, and 6.7 ng per 10(6) mastocytoma cells within 5 min at 37 degrees C, which was maintained for up to 45 min. The maximum production of leukotrienes by mastocytoma cells activated with optimum concentrations of 0.2 to 1 microM calcium ionophore A23187 was 35% to 50% greater than that achieved by antigen challenge, without alterations in the relative quantities of leukotrienes, but was realized only after 30 min at 37 degrees C. The leukotriene products of mastocytoma cells were identified by high-performance liquid chromatography, spectral properties, and immunoreactivity with mono-specific antisera, and exhibited the same concentration-dependence of biologic activity as authentic synthetic standards. The ratio of quantities of C-6 peptide leukotrienes generated was attributable in part to the rate of peptidolytic conversion of LTC4 to LTD4 in the mastocytoma cells, which was 33% per 30 min at 37 degrees C. The rapid maximum response to IgE-dependent stimulation and the unique spectrum of products distinguishes the secretion of leukotrienes by dog mastocytoma cells from that by basophils and some other types of mast cells and suggests diverse contributions of mast cell leukotrienes to immediate and late hypersensitivity reactions.
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PMID:IgE-dependent and ionophore-induced generation of leukotrienes by dog mastocytoma cells. 630 9

A heat-sensitive (hs, arrested at 39.5 degrees C, multiplying at 33 degrees C) and a cold-sensitive (cs, arrested at 33 degrees C, multiplying at 39.5 degrees C) cell cycle variant were isolated from an undifferentiated P-815 murine mastocytoma line. At the respective nonpermissive temperature, both the hs and the cs variant cells were reversibly arrested with a DNA content, typical of G1 phase. The cells of two cs variant subclones, when exposed to the nonpermissive temperature of 33 degrees C, formed metachromatically staining granules with an ultrastructure resembling that of mature mast cells. In addition, the cellular 5-hydroxytryptamine content underwent a marked increase, and the cells responded to compound 48/80 by degranulation as described for normal mast cells. On the other hand, in cells of two hs variant subclones, essentially no mast cell granules were detectable at either 33 or 39.5 degrees C. As previously reported, the cs cell cycle variant phenotype is expressed dominantly in heterokaryons obtained by fusing cs with wild-type cells, whereas hs cell cycle variant cells, similar to other hs mutants, were found to behave recessively under these conditions. Thus the state of proliferative quiescence induced in the cs cells at 33 degrees C is qualitatively different from the state of cell cycle arrest observed in hs cells at 39.5 degrees C and may represent a model for proliferative quiescence of differentiated cells in the intact organism.
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PMID:Formation of mast cell granules in cell cycle mutants of an undifferentiated mastocytoma line: evidence for two different states of reversible proliferative quiescence. 640 19

Mastocytoma was diagnosed in a four year old Holstein cow. The enlarging mass was clinically determined to be metastatic to the right superficial cervical lymph node. Cytological examination of both sites revealed mast cell neoplasia. Histopathological examination confirmed the presence of this tumor in these same sites as well as in liver, kidney and adrenal. Ultrastructurally, the mass contained round cells with electron dense granules in the cytoplasm.
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PMID:Mastocytoma in a cow: a case report. 642 14


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