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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 are widely distributed in perivascular connective tissues, especially in areas of active tumor growth and vascular reactivity. Incubation of metabolically [35S]O4 = -labeled subendothelial extracellular matrix (ECM) with lysates of bone marrow-derived mouse mast cells (BMMC) resulted in extensive degradation of heparan sulfate (HS) into fragments 5 to 6 times smaller than intact HS side chains. A much lower activity (seven- to eightfold) was expressed by intact BMMC incubated in contact with the ECM. These fragments were not produced in the presence of heparin, were sensitive to deamination with nitrous acid, and resistant to further degradation with papain or chondroitinase ABC. These results indicate that an endoglycosidase (heparanase) is involved in BMMC-mediated degradation of HS in the subendothelial ECM. Heparanase activity was not detected in medium conditioned by cultured BMMC, or in lysates of Ableson transformed BMMC and rat basophilic leukemic (RBL) cells. Both heparanase and beta-hexosaminidase, a mast cell granule enzyme, were released on degranulation of BMMC induced by the calcium ionophore A23187, or by exposure to IgE-Ag, suggesting that heparanase is localized in the cell granules. Under these conditions, less than 5% of the cellular content of lactate dehydrogenase were released. Degradation of the ECM-HS by the mast cell heparanase and the associated release of HS-bound endothelial cell growth factors that are stored in ECM (Vlodavsky et al, Proc Natl Acad Sci USA 84:2292, 1987; Bashkin et al, Biochemistry 28:1737, 1989) may play a role in the proposed mast cell-mediated stimulation of neovascularization.
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PMID:Degranulating mast cells secrete an endoglycosidase that degrades heparan sulfate in subendothelial extracellular matrix. 169 99

Mast cells are primarily localized in connective tissues, where they secrete numerous mediators. They have also been identified in the mammalian central nervous system on the basis of their histochemical and morphological properties, but their role there remains unknown. A perfusion system was used to investigate in vitro mediator release from rat brain mast cells. Compound 48/80, the classic mast cell secretagogue of connective tissue mast cells, induced dose-dependent and non-cytotoxic release of serotonin, histamine and beta-hexosaminidase from mast cells in the rat thalamus and hypothalamus, but not in the cerebellum which was used as a negative control. Detailed studies were performed on thalamic mast cells, which were identified on the basis of metachromasia with Toluidine Blue and Safranin-positive staining with the Alcian Blue/Safranin technique. Their secretion was characterized by: (a) parallel release of serotonin, histamine and beta-hexosaminidase; (b) lack of dependence on extracellular calcium; (c) susceptibility to inhibition by disodium cromoglycate; and (d) lack of lactate dehydrogenase release. These results indicate that the morphology and secretory characteristics of thalamic mast cells resemble those of connective tissue mast cells. The ability of brain mast cells to secrete their mediators is discussed in the context of their possible involvement in brain pathophysiology.
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PMID:Serotonin release from rat brain mast cells in vitro. 170 65

To test whether bile acids interact with mast cells, dilute, aqueous solutions of five pure unconjugated natural bile acids and their corresponding glycine or taurine conjugates were incubated with murine PT-18 cells (a mast cell line functionally and cytochemically similar to mucosal mast cells) or with freshly isolated rat peritoneal mast cells. Bile acid solutions ranged in concentration from 0.3 to 10 mmol/L; histamine release was assessed by a fluorimetric assay, and cell lysis by cytosolic enzyme (lactate dehydrogenase) release. Lipophilic, dihydroxy bile acids (chenodeoxycholic acid and deoxycholic acid as well as their glycine and taurine conjugates) caused histamine release in a dose-related manner; cholic acid and its conjugates caused much less or no histamine release. Two hydrophilic bile acids (ursodeoxycholic acid and ursocholic acid and their conjugates) were virtually devoid of activity. Histamine release, which was independent of extracellular Ca2+, occurred at 0.3 mmol/L, well below the critical micellization concentration. For a given concentration, unconjugated bile acids and glycine-conjugated bile acids induced more histamine release than taurine-conjugated bile acids; maximal release was observed at 3 mmol/L for lipophilic, dihydroxy bile acids. To test whether bile acids could also cause histamine release from cutaneous mast cells in vivo, rats were injected intradermally with bile acid solutions and histamine release assessed by capillary leakage of Evan's blue dye. Cutaneous blueing was greater with cytotoxic bile acids, chenodeoxycholyglycine or deoxycholylglycine, than with ursodeoxycholylglycine and was inhibited by prior antihistamine treatment. Histamine release correlated highly and positively with lipophilicity and with bile acid surface activity. It was concluded that lipophilic but not hydrophilic bile acids possess concentration-dependent cytotoxicity toward mast cells causing histamine release, that unconjugated and glycine-conjugated bile acids are more potent than taurine-conjugated bile acids, and that mast cell histamine release is highly correlated with lipophilicity of bile acids as well as their surface activity.
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PMID:Activation of mast cells by bile acids. 171 30

In an ischemia-reperfusion model obtained in isolated perfused guinea pig heart by means of a double ligature of the left anterior descending coronary artery, the reperfusion of the ischemic myocardium leads to a release of lactate dehydrogenase and histamine, related to a decrease in the microdensitometry of cardiac mast cells and to a tissue calcium overload. The perfusion of the heart with L-arginine and with nitric oxide donors significantly reduces the release of histamine, the loss of mast cell metachromasia and calcium overload. These effects were potentiated by superoxide dismutase.
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PMID:Effect of nitric oxide generators on ischemia-reperfusion injury and histamine release in isolated perfused guinea pig heart. 171 88

A transient increase in the permeability of the mast cell membrane was caused by the exposure of the cells to low concentrations of saponin, 5 or 10 micrograms/ml. These concentrations had very little effect in the absence of calcium but caused 35 to 50% histamine release, having the character of a secretory response, when 0.25 mM or more calcium was added to the medium. The dose-response curve was steep between 25 microM and 250 microM calcium and tended to flatten with higher concentrations. The release was associated with a pronounced increase in calcium uptake, which was faster than the histamine release. The membrane changes were slight as indicated by only 7 to 12% leakage of lactate dehydrogenase and by the absence of any detectable change in the electron micrographs. The transient nature of the membrane change is shown by the following experiment. When the cells were first exposed to saponin in the absence of calcium, the amount of histamine released by the subsequent incubation with calcium varied inversely with the time interval that elapsed before calcium was added. If calcium was added after 15 minutes no histamine release occurred. When calcium uptake was studied in the same manner, the stimulation of calcium uptake in saponin-treated cells also declined progressively with increasing intervals after the exposure to saponin when calcium was added. Stimulation of both histamine release and calcium uptake was inhibited by antimycin A, the inhibition curves with 10(-9)M to 10(-7)M antimycin A being similar. The effect on the calcium uptake by itself could explain the inhibition of histamine release. But the release was also inhibited by the calmodulin antagonists, W-7 and mepacrine, suggesting that the influx of calcium in the permeabilized cells acts primarily through calmodulin-mediated enzyme activation.
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PMID:Histamine secretion from permeabilized mast cells by calcium. 242 33

Rat peritoneal mast cells have been permeabilised by treatment with streptolysin O which generates membrane lesions of macromolecular dimensions. In the presence of Ca2+ buffered at concentrations in the micromolar range, the permeabilised mast cells release histamine, beta-N-acetylglucosaminidase and lactate dehydrogenase. Release of the two secretory components (but not lactate dehydrogenase) has an obligatory requirement for a nucleoside triphosphate and micromolar concentrations of Ca2+. Inosine triphosphate (ITP) supports the release reaction better than ATP does. It is concluded that the secretory materials are released from the cells by an exocytotic mechanism, while lactate dehydrogenase leaks from the cells through the toxin-generated lesions. By initially withholding and then supplying Ca2+ to the permeabilised cells, it is shown that the exocytotic secretory reaction can persist even when the cytosol is depleted of the bulk of soluble proteins. The streptolysin O treated mast cell preparation represents a simplified system with which to study the mechanism of exocytosis.
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PMID:Rat mast cells permeabilised with streptolysin O secrete histamine in response to Ca2+ at concentrations buffered in the micromolar range. 243 36

In the present paper we report the results of experiments carried out to measure the release of histamine from isolated rat mast cells during the metabolic activation of arachidonic acid. Arachidonic acid (10(-8)-10(-4) M) and the terminal products (10(-6) M) of the arachidonic acid pathways were devoid of any significant histamine releasing properties. A substantial amount of histamine was released from rat mast cells by low concentrations of arachidonic acid during incubation with prostanoid generating systems, such as guinea-pig lung microsomes, rat serosal macrophages and polymorphonuclear cells and prostaglandin-H-synthase from calf seminal vesicles. The release of histamine was not accompanied by a leakage of lactate dehydrogenase and was blocked by D-mannitol and by lipoxygenase and cyclooxygenase pathway inhibitors. The data are consistent with the hypothesis that free radical derivatives of arachidonic acid, originating from hydroperoxy fatty acids, are generated during catalysis, causing mast cell histamine release.
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PMID:Histamine release from serosal mast cells by intermediate products of arachidonic acid metabolism. 244 Feb 71

Histamine has been proved to be released during myocardial infarction and ischemic arrhythmias in dogs. The aim of the present experiments was to evaluate if ischemia and reperfusion modify histamine and lactate dehydrogenase (LDH) release in isolated guinea-pig heart. The results obtained show a steady increase of LDH release both in the ischemic and reperfusion phases. The release of histamine was reduced during the ischemic phase and increased significantly during reperfusion. A significant diminution of mast cell granule metachromasia was observed in the right auricles at the end of the reperfusion period. D-mannitol and reduced glutathione (GSH) modified the kinetics of histamine and LDH release. Cimetidine was able to decrease significantly the release of histamine during the ischemic and reperfusion phases and also reduced the release of LDH; triprolidine was completely ineffective. The results suggest that oxygen-derived free radicals may be involved in the pathogenesis of myocardial dysfunction after ischemia and reperfusion.
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PMID:Histamine and lactate dehydrogenase (LDH) release in ischemic myocardium of the guinea-pig. 244 Feb 79

It has been shown that plasma histamine significantly increases during myocardial infarction in the dog. Histamine is also released when the isolated guinea-pig heart is reperfused after 30 minutes of low flow perfusion. The release of histamine and lactate dehydrogenase (LDH) after left anterior descending coronary artery ligation and release were investigated in the present study and related to the changes in electrocardiographic parameters and to a computer-aided analysis of left ventricular mast cell metachromasia. Spontaneous release of histamine was unchanged during ischemia and increased after the release of the ligature, while we observed a steady increase of LDH overflow. In parallel, a significant diminution of mast cell granule metachromasia was observed in left ventricular samples. The perfusion of the heart with FeCl3/ADP (10 microM/100 microM), a free radical-generating system, significantly enhanced both the basal and ischemic-reperfusion release of histamine, while perfusion with N-t-butyl-phenyl-nitrone (BPN/100 microM) a "spin-trapper" molecule, significantly decreased histamine and LDH release and the loss in metachromasia of left ventricular mast cells induced by reperfusion. Inhibitors of xanthine oxidase (allopurinol, 10 microM) and of calcium-activated proteases (leupeptin, 10 microM) modified the kinetics of histamine and LDH release.
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PMID:Histamine release in acute coronary occlusion-reperfusion in isolated guinea-pig heart. 245 99

The effects of synthetic polycations, which induce liposomal membrane fusion without inducing permeability changes, on histamine release from rat mast cells were investigated. Polyethylenimines and polyallylamines with various molecular weights released histamine from mast cells. Acetylated derivatives and triethylentetramine did not release histamine or serotonin from the cells. The histamine release induced by 10 micrograms/ml polyethylenimine with a molecular weight of 600 was inhibited by 1 mM dibutyryl cyclic AMP, but not by 1 MM 8-bromo cyclic GMP; 100 microM D-600, a calcium antagonist; or 30 microM W-7, a calmodulin inhibitor. In the presence of polyethylenimines with molecular weights of 600, 1,200 and 1,800, no detectable release of cytosolic lactate dehydrogenase was observed, indicating that histamine release induced by these polycations was not due to their cytotoxicity. The potencies of these polymers in inducing histamine release depended on their charges, but not on their degrees of polymerization. On the other hand, the actions of polyethylenimine with a molecular weight of 10,000 and polyallylamines with molecular weights of 3,000-4,000 and 10,000 in releasing lactate dehydrogenase were somewhat cytotoxic. These polycations did not induce serotonin release from rat platelets, suggesting that platelets have no coupling system of signal transduction by these polycations. Thus polycations seemed to interact with the mast cell membrane to induce histamine release, and the potencies of these polycations on mast cells seemed to differ from those of their effects on liposomes, which were examined previously.
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PMID:Synthetic polycations, polyethylenimines and polyallylamines release histamine from rat mast cells. 248 Apr 66


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