Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mast cell population of rat diaphragm was estimated between birth and adulthood and found to rise with an increase in the age of rat studied. Degranulation of these cells was observed in rats from all age groups, following treatment with compound 48/80 and dextran. The association of mast cells with the blood vessel wall in adult rat diaphragm was not observed in the comparable tissues of newborn rats. These findings are discussed in relationship to the poor vascular permeability reactions exhibited by newborn and young rats.
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PMID:The mast cells of the newborn rat diaphragm and their response to histamine liberators. 5 89

Inhibitors of mast cell membrane activation reduced histamine release from rat mast cells induced by dextran and phosphatidyl serine but not that induced by the calcium ionophore A23187. Such inhibitors included cromoglycate, an orally-active anti-allergic agent 3-(5-tetrazolyl)thioxanthone 10,10-dioxide, dibutyryl cyclic 3':5'-AMP, theophylline and dicumarol. Inhibitors of mast cell metabolism reduced both types of release and these included oligomycin, papevevime, and the two uncouplers of oxidative phosphorylation-alpha2,4-dinitrophenol and CCCP. Inhibition of histamine release from rat isolated peritoneal mast cells by either a mixture of dextran and phosphatidyl serine or the ionophore A23187 thus allows inhibitors of mast cell membrane activation to be distinguished from those affecting cell metabolism or the later stages of the secretory process.
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PMID:Differential histamine release by dextran and the ionophore A23187: the actions of inhibitors. 5 25

Alpha-chymotrypsin (CT) was modified chemically and physically by the treatments with diisopropyl fluorophosphate, L-(1-tosylamide-2-phenyl) ethylchloromethylketone, hydrogen peroxide and heat. After these treatments, CT lost or decreased both the enzymic activity and ability of releasing histamine from rat mast cells. Ca++ was essential for histamine release by CT, while it enhanced only slightly the enzymic activity. Process of histamine release by CT could be separated into two stages: CT-dependent but not Ca++-dependent, and Ca++-dependent but not CT-dependent. The activated state of mast cells produced by CT decayed rapidly at 37 degrees C in the absence of Ca++, but these cells responded to Ca++ by adding CT once again, suggesting reconstitution of cell membrane structure affected by CT. Isoproterenol, epinephrine, prostaglandin E1, and dibutyryl-cyclic AMP (0.01-0.1 mM) did not inhibit release of histamine induced by CT. Neither theophylline (0.01-0.1 mM) alone nor the combinations of these cyclic AMP-active agents with theophylline inhibited the release of histamine. But, in the presence of papaverine (0.01-0.1 mM) a marked, dose-dependent inhibition was observed. These data suggest that 1) release of histamine by CT from rat mast cells is causally related to its hydrolytic activity, 2) this activity causes a reversible change on mast cell membrane which probably facilitates Ca++-influx through the cell membrane, and 3) there are subtle differences among CT, compound 48/80 and antigens concerning the effect of cyclic AMP-active agents in histamine-releasing mechanisms in mast cells.
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PMID:Mechanism of histamine release by alpha-chymotrypsin from isolated rat mast cells. 5 33

We have attempted to review the current state of our knowledge concerning the human basophilic leucocyte, drawing on experimental data derived from animals when necessary. Long neglected, a great deal has been learned about these cells in recent years, about their morphology, their biochemical constitutents and their ability to synthesize certain of these constitutents, their interactions with homocytotropic antibodies, their release of mediators in anaphylaxis, their response to chemotatic stimuli, their participation and progressive degranulation in cell-mediated hypersensitivity reactions, and their capacity for ingesting and releasing certain exogenous tracers. Despite this vast accumulation of new information, much more must be learned before we can confidently describe the role of basophils, or of the closely related mast cells, in health or disease. It seems most unlikely that either cell exists for the purpose of destroying the organism in anaphylactic shock. Nonetheless, it is highly probably that basophil/mast cell function is closely related to the potent chemicals stored within their cytoplasmic granules. One likely possibility holds that small amounts of these chemicals are required for homeostasis (e.g., for regulation of the tone of the microvasculature) and that these cells function by releasing such substances continuously, as they are needed, in small aliquots rather than by explosive discharge. This hypothesis requires that basophils be capable of releasing their contents in piecemeal fashion. Such gradual release apparently occurs in delayed-type hypersensitivity reactions, but the mechanisms responsible for this form of degranulation have not yet been identified. This hypothesis also requires that physiological, rather than pharmacological, roles be found for histamine, heparin and possibly for other components of the basophils/mast cell granules. Progress in this direction has been extremely slow.
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PMID:Basophilic leucocytes: structure, function and role in disease. 5 13

In the presence of L-cysteine, a selective and marked enhancement of the in vitro, immunologic release of slow reacting substance of anaphylaxis (SRS-A) from human peripheral leukocytes, sensitized monkey lung fragments, and sensitized guinea pig lung fragments was observed. In the rat, cysteine, but not sodium sulfide, enhanced the calcium ionophore (A23187)- induced release of SRS-A in vitro from mixed rat peritoneal cells and in vivo from the rat peritoneal cavity. Pretreatment of rats with cysteine also enhanced the IgGa-and anti-rat IgE-mediated release of SRS-A in vivo in the rat. These studies indicate a common biochemical mechanism involved in the formation and release of SRS-A from these different tissues and cells and further confirm the observation that the rat mast cell is not a major source of SRS-A in the rat.
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PMID:The effect of thiols on the immunologic release of slow reacting substance of anaphylaxis. II. Other in vitro and in vivo models. 5 39

Patients with idiopathic acquired cold-induced urticaria were evaluated for the release of the preformed mast-cell mediators of immediate-type hypersensitivity during a study in which one arm was immersed in ice water while the other arm remained as a control. Blood specimens were obtained from each arm serially over a one-hour interval, and serum speciments were assessed for histamine, eosinophil chemotactic factor of anaphylaxis, and complement components. Levels of histamine and eosinophil chemotactic factor rose in the arm subjected to cold immersion for three minutes, with peak values occurring between two and five minutes and returning to base line by 30 minutes. No changes occurred in the control arm or in the immersed arm of normal subjects. Assessment of the classical and alternative complement pathways showed no abnormalities. This initial observation of release of eosinophil chemotactic factor of anaphylaxis in vivo along with histamine assigns the mast cell a central role in cold urticaria.
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PMID:Cold urticaria: release into the circulation of histamine and eosinophil chemotactic factor of anaphylaxis during cold challenge. 5 69

The release of exogenous histamine was studied by superfusing brain slices following incubation with the radiolabeled amine. Histamine was released in a calcium-dependent way by 40 mM potassium. This release was high in hypothalamus and striatum and low in hippocampus and cortex. Compound 48/80, a mast cell histamine releasing agent, also induced histamine release, but only from hypothalamic tissue slices. It is suggested that the potassium-induced release of accumulated exogenous histamine is mainly from glial cells.
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PMID:Potassium-induced release of tritiated histamine from rat brain tissue slices. 5 72

In a series of tests designed to illustrate immune reactions similar to those obtained in atopic disease, Wy-16,922 effectively inhibited reaginic-mediated immunologic reactions in the skin, longs and mast cell. It was found to be devoid of immunosuppressant, antimediator, anti-inflammatory, steroid or bronchodilator properties as well as acute toxicity. Although the mechanism of action Wy-16,922 is unknown, it appears to limit the release (not the effects) of allergic mediators in a manner similar to that described for disodium cromoglycate.
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PMID:Immunopharmacologic properties of WY-16,922, a new orally effective antiallergic agent. 5 34

Mast cells were examined from various sites in the normal human stomach and in the stomachs of patients with gastric ulceration. The distribution of the different types of mast cell granules was determined in the subepithelial region of the normal human stomach. There was a significant difference in this respect between the mast cells at the incisura angularis as compared with those high on the lesser curve or high on the greater curve. Mast cell degranulation (i.e. the shedding of intact granules) and vacuolation were examined with the electron microscope. Degranulation and vacuolation were observed in subepithelial mast cells, whereas only vacuolation was seen in intraepithelial mast cells. The significance of degranulation and vacuolation is discussed.
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PMID:Mast cells of the human stomach. 5 56

Rabbits were immunized with rat peritoneal mast cells (RMC) in complete Freund's adjuvant. The antisera (anti-RMC) were checked for their reactivity with RMC by intradermal skin tests in rats. The best serum was selected and absorbed with rat liver cells and rat immunoglobulins, including IgE. The absorbed serum (anti-RMCabs), as well as the anti-RMC serum, were then tested for their reactivity with RMC. Both sera were cytotoxic to RMC but only anti-RMC was cytotoxic for rat lymph node cells. Both sera gave positive reactions in rat skin, as seen by the permeability to Evan's blue dye. The binding of rat IgE to RMC was also inhibited by both sera. A control rabbit anti-rat sarcoma serum absorbed with liver cells did not show any interaction with RMC. When 125I-labeled RMC surface antigens were precipitated with anti-RMCabs and analyzed by SDS polyacrylamide gel electrophoresis, several components were observed. Among these was one with a mobility identical to that of a mast cell surface component that had previously been identified as the receptor for IgE or at least a component thereof.
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PMID:Characterization of an antiserum specific for cell surface antigens of rat mast cells. 5 33


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