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

The biogenic amines and heparin of rat peritoneal mast cells were labelled in vivo by the injection of amine precursors (3H-histidine and 3H-5-hydroxytryptophan) and 35S-sodium sulfate. Uptake of label was rapid, probably reflecting the synthesis of new granule material, but the elimination was slow. Half-lives of radiolabelled histamine (23 days) and 5-hydroxytryptamine (5-HT; 25 days) did not differ statistically from that of heparin (35 days). The slow elimination rates suggest that mast cell secretion is of little biological significance under normal conditions but are well compatible with the idea that mast cell function is related to secretion evoked by appropriate immunological stimuli. It further permitted an analysis of the amine storage by repeated injections of unlabelled 5-HT. A 15-fold increase in 5-HT content was obtained while the total amine content remained constant. The uptake of 5-HT was balanced by a reduction of histamine in a molar 1:1 ratio. A displacement of histamine by 5-HT was further indicated by increased elimination rate of radiolabelled histamine in response to 5-HT injections. The results support previous binding studies in vitro and indicate that histamine and 5-HT are bound to identical storage sites in the mast cell granules.
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PMID:Storage and turnover of histamine, 5-hydroxytryptamine and heparin in rat peritoneal mast cells in vivo. 682 30

The intravenous injection of the mast cell degranulator C 48/80 (1 mg/kg) in rats did not produce thrombocytopenia nor circulating platelet aggregates but sensitized the platelets to aggregate upon turbulence challenge. Such turbulence-induced platelet aggregation was not accompanied by formation of thromboxane B2. Electron microscopy revealed absence of platelet degranulation. Turbulence-induced platelet aggregation was completely prevented by pre-treatment of the rats with cyproheptadine, dipyridamole and VK 774, partially with ketanserin (5HT2-receptor antagonist), but not with methysergide (antiserotonergic drug), pyrilamine (antihistaminic drug), suprofen, aspirin (cyclo-oxygenase inhibitors), phentolamine, propranolol, flunarizine, lidoflazine, oxycoumarin or Trasylol. Combined treatment with the anti-histaminic drug pyrilamine and the 5HT2-receptor antagonist ketanserin resulted in a dose-related inhibition for ketanserin of the turbulence-induced platelet aggregation. These experiments point to an interaction between histamine and 5-hydroxytryptamine in the platelet activation by mast cell released mediators.
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PMID:Platelet activation by endogenous 5-hydroxytryptamine and histamine released by mast cell degranulation with compound 48/80 in the rat. 685 90

For individual mast cells, relationships between their dry mass and their content of heparin and 5-hydroxytryptamine (5-HT) were studied. This was achieved by measuring these parameters successively on identical cells, by means of quantitative cytochemical techniques. The peritoneal mast cells have a very long life span and a slow turnover of granule components. Increase of the dry weight of the cells may therefore be taken as an expression of cellular growth. Mast cell populations from younger and older animals were analysed in an attempt to evaluate the influence of cell-aging and animal-aging on the growth of the mast cells. The analysis was based on allometric (log-log) plots and linear regressions. Within the cell populations there were strong mutual correlations between the cell parameters studied, without any obvious deviations from linearity. However, the slopes of the allometric lines indicated a somewhat different mode of growth for mast cell from younger and older animals. The capacity of the mast cells to accumulate 5-HT after a single injection of its precursor, 5-hydroxytryptophan, was used as a functional test. In relation to the cell weight, the induced increase of 5-HT was greater for lighter than for heavier mast cells. This difference between light and heavy mast cells was greater for cells from younger than from older animals. These differences in growth and functional properties between mast cells from younger and older animals were interpreted as an effect of the animals rather than of aging of the cells.
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PMID:A quantitative cytochemical study of the growth of individual mast cells. 696 55

We have previously suggested that the release of serotonin (5-hydroxytryptamine) (5-HT) by local tissue mast cells is required for the elicitation of delayed-type hypersensitivity (DTH) in mice. In the current study, light microscopic radioautographs from animals treated with [3H]5-HT indicated that local mast cells released 5-HT between 6 and 18 h during the evolution of DTH. Ultrastructural examination of mast cells revealed surface activation, indicated by extension of surface filopodia, and degranulation by fusion and exocytosis. Light and electron microscopic studies of the endothelium of postcapillary venules at sites of DTH revealed the development of gaps between adjacent cells. The development of gaps permitted extravasation of tracers that was abolished by depletion or antagonism of 5-HT. Thus mast cells degranulated and released 5-HT in DTH, and this 5-HT acted on local vessels. Recipients of nonadherent, non-immunoglobulin-bearing sensitized lymphocytes also demonstrated similar mast cell degranulation and the formation of endothelial gaps. This indicated that mast cell degranulation and 5-HT release in murine DTH were probably T cell dependent.
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PMID:T cell-dependent mast cell degranulation and release of serotonin in murine delayed-type hypersensitivity. 696 11

Uptake and turnover of dopamine (DA) in rat peritoneal mast cells were studied by a cytofluorometric technique. The main advantage of the method is that it permits the study of the distribution of amine content within populations of cells. Catecholamines and indolamines can be differentiated, but subtler structural differences in this group of compounds cannot be distinguished. We, therefore, combined the cytofluorometric measurements with a liquid chromatographic method based on reversed-phase chromatography followed by amperometric detection in a thin layer flow cell. Intraperitoneally injected L-DOPA was rapidly decarboxylated to DA, which was accumulated in mast cell granules. The elimination of DA from the mast cells was much faster than previously published 5-hydroxytryptamine and histamine elimination rates. No evidence of intracellular conversion of DA before its elimination was found and simultaneous heparin quantitations gave no evidence of an elimination pathway due to exocytosis of granules. Electron microscopy disclosed no structural changes that could be related to exocytosis during the elimination phase of DA. The rapid elimination together with absence of inhibition of DA-uptake after storage of exogenous 5-hydroxytryptamine suggest that the mechanism of DA storage differs from the mechanism of storage of endogenous mast cell amines.
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PMID:Uptake and turnover of dopamine in rat mast cells studied by cytofluorometry and high performance liquid chromatography. 711 68

Two types of inhibition of basic peptide-induced rat mast cell secretion are reported. Pretreatment of rat peritoneal mast cells with Vibrio comma neuraminidase, an enzyme which cleaves sialic acid from oligosaccharides, led to inhibition of 5-hydroxytryptamine release induced by the basic peptides polylysine, corticotropin 1-24 and a decapeptide sequence of human IgE. Inhibition was similarly observed when mast cells were challenged in the presence of the cationic cell membrane-active substance benzalkonium chloride. It is postulated that both of these experimental procedures inhibit basic peptide-induced secretion by depletion of cell surface negative charge. Sialic acid itself does not act as a specific receptor for basic peptides, since a molar excess of sialic acid in free solution failed to inhibit secretion by binding to basic peptides in the fluid phase.
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PMID:Neuraminidase- and benzalkonium chloride-dependent inhibition of basic peptide-induced rat mast cell secretion. 717 80

The histamine and 5-hydroxytryptamine (5-HT) content of mast cells was measured in rat peritoneal mast cells (isolated by density-gradient centrifugation or in crude peritoneal cell suspensions) and in some solid, mast-cell-rich tissues (tongue, skin, and duodenum). The duodenum contains large numbers of mast cells belonging to the specific type of mucosal mast cell. The peritoneal cavity, tongue, and skin contains the classical, mature connective-tissue-type of mast cell. The approximate amine content in mast cells of solid tissues was calculated by combining the biochemical assays with cell counting. The amine content was related to the age and body weight of the rats, studied during a period of rapid body growth (25-233 days). In the connective-tissue-mast cells both amines showed an increase that was strongly correlated to age and body weight. The increment of histamine was not as large as that of 5-HT. In peritoneal mast cells the histamine content per cell was doubled during the growth period studied, whereas there was a sixfold increase of 5-HT. The estimated 5-HT content per mast cell of tongue and skin also increased in relation to body weight. The histamine/5-HT quotients in these tissues were similar, and decreased with increasing age as did the same quotients for peritoneal cells. Parallel cell counts and histamine assays indicated that the mucosal mast cells contained much less histamine than the connective-tissue mast cells, and this findings was supported by histochemical observations. The observations did not suggest that histamine is stored else-where than in mast cells. In the mucosal mast cells, too, the histamine content appeared to increase as a function of age and body weight. Duodenal 5-HT, which is to a large extent contained in enterochromaffin cells, did not increase in relation to body growth.
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PMID:Histamine content of peritoneal and tissue mast cells of growing rats. 739 Aug 77

Nedocromil sodium is commonly suggested to reduce allergic inflammation by inhibiting mediator release from mast cells. However, nedocromil also exhibits a wide range of additional anti-inflammatory activities, including inhibition of increased vascular permeability induced by individual mediators such as histamine. In the present study, we have further characterized the mode of action of nedocromil in a rat model for hind paw edema. Mast cell-dependent edema was induced with compound 48/80 (edema response mainly due to 5-hydroxytryptamine release), and direct mediator-induced plasma extravasation was evoked by exogenous 5-hydroxytryptamine (both agents injected locally). Local pretreatment with nedocromil for 20 min dose-dependently inhibited the edema evoked by compound 48/80 more effectively than that induced by 5-hydroxytryptamine. However, after 2 h pretreatment, both the 5-hydroxytryptamine-and compound 48/80-induced edema responses were inhibited to approximately the same extent by a range of concentrations of nedocromil, as well as by dexamethasone. Local inhibition of RNA/protein synthesis with actinomycin-D abolished the effects of both dexamethasone and nedocromil (2 h local pretreatment). We thus conclude that nedocromil can produce an 'anti-exudative' effect that is independent of inhibition of mast cell mediator release, is slow in onset, and requires de novo protein synthesis.
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PMID:Delayed anti-inflammatory action of nedocromil sodium in the rat paw is dependent on de novo protein synthesis. 749 78

Nitro-L-arginine methyl ester (0.15 mumol/paw) significantly reduced both bradykinin- and 5-hydroxytryptamine-induced rat paw oedema. At this dose, L-arginine (L-Arg), D-Arg and nitro-D-arginine methyl ester had no effect on the oedematogenic responses induced by these agents. Nitro-L-arginine methyl ester, nitro-D-arginine methyl ester, L-Arg, D-Arg, L-arginine methyl ester and L-arginine ethyl ester, at the dose of 15 mumol/paw, significantly potentiated both bradykinin- and 5-hydroxytryptamine-induced oedema. This potentiation was not observed in animals treated with both mepyramine and methysergide or in animals chronically treated with compound 48/80. Nitro-L-arginine methyl ester (0.3-3 mM) and L-Arg (0.3-3 mM) released small amounts (< 10%) of histamine from rat peritoneal mast cells when compared to compound 48/80-induced degranulation (> 40%). Histamine release was quantified by radioimmunoassay since nitro-L-arginine methyl ester and L-Arg interfere with the fluorometric assay. The potentiation of paw oedema observed with higher doses of all arginine analogues is caused by in vivo mast cell degranulation and is probably due to the cationic charge of these substances.
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PMID:Effect of arginine analogues on rat hind paw oedema and mast cell activation in vitro. 752 38

As studied by intravital microscopy, local challenge with the mast cell secretagogue compound 48/80 was found to increase the leukocyte rolling fraction, decrease rolling velocity and induce firm leukocyte adhesion in postcapillary venules of the rat mesentery. These effects of compound 48/80 were inhibited by a monoclonal anti-P-selectin antibody, but not by combined treatment with H1 and H2 histamine-receptor antagonists. Moreover, the response to compound 48/80 was not mimicked by exogenous histamine or 5-hydroxytryptamine (5-HT). These novel findings indicate that mediator(s) other than histamine and 5-HT evoke P-selectin-dependent leukocyte rolling and thereby promote firm leukocyte adhesion in mast cell-dependent inflammation.
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PMID:Mast cell activation induces P-selectin-dependent leukocyte rolling and adhesion in postcapillary venules in vivo. 752 40


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