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

The effects of atropine, mepyramine, metiamide or NaHCO3 on gastric ulceration, gastric secretion and gastric mast cell degranulation were studied in stressed pylorus-occluded rats. The influence of dexamethasone pretreatment on stress ulcers in animals without pylorus occlusion (intact rats) was also examined. Stress produced a high glandular lesion incidence and ulcer index, and markedly lowered gastric secretion and glandular wall mast cell counts. Injected 0.5 h before stress, atropine, mepyramine or metiamide strongly antagonised ulceration. Atropine or metiamide, but not mepyramine, reduced gastric secretion. Only atropine prevented stress-induced mast cell changes. NaHCO3, given intragastrically before stress, did not prevent ulceration or mast cell degranulation despite complete neutralisation of gastric acid. Dexamethasone-induced gastric mucosal mast cell depletion could reduce stress ulceration. The findings show that stress degranulates stomach mast cells via a cholinergic pathway; released histamine from this source is largely responsbile for gastric ulceration through H1- and H2-receptor effects. Histamine H2-receptor-mediated gastric acid may play only a small contributory role in stress ulcers in rats. The antiulcer mechanisms of histamine H1- and H2-receptor blockade are discussed.
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PMID:Cholinergic-mediated gastric mast cell degranulation with subsequent histamine H1-and H2-receptor activation in stress ulceration in rats. 43 42

The patterns of distribution of histamine and norepinephrine among the 4 chambers of the heart of rats, guinea pigs, and rabbits and among 15 portions of the dog heart were quite similar, except for the coronary ring of the dog, which was disproportionately high in histamine. In whole mouse hearts the separate chambers were not assayed; in the whole heart, the contents of the 2 amines did not correlate. The subcellular distribution of histamine in the rat and guinea pig heart was different from that of norepinephrine. Histamine was mostly associated with mast cell-like granules. Toluidine blue-staining granules of 2 widely different densities were found.
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PMID:Comparative regional and subcellular distributions of histamine and norepinephrine in the hearts of rats, mice, guinea pigs, rabbits, and dogs. 65 Aug 92

1. Histamine was detected in the abdominal aorta and the femoral arteries of normotensive and also DOCA-hypertensive rats. 2. Levels of total histamine (mast cell and non-mast cell histamine) were significantly reduced in both abdominal aorta and the femoral artery of the DOCA-hypertensive rats, relative to the normotensive controls. 3. It is suggested that the diminished level of vascular histamine may be related to the development and/or maintenance of the hypertensive state and is also related to the reduced magnitude of active reflex vasodilatation.
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PMID:Alterations in levels of vascular histamine in the DOCA-hypertensive rat. 69 85

Histamine has been found biochemically in the mammalian vascular wall. This study was undertaken in an effort to identify the presence of specific histamine-containing cells inwalls of large blood vessels such as femoral artery and vein, brachial artery and vein, mesenteric artery and vein, renal artery and vein, and aorta. Segments of vessels from rats, cats, dogs, sheep, cows, humans and chickens were examined. Sections were prepared from fresh tissue by vibratome, from frozen tissue by cryostat and from freeze-dried and fixed tissues. Mast cells were visualized by staining with acidic toluidine blue and by reaction with orthophthaladehyde to develop histamine fluorescence. Although mast cells were easily identified in preparations such as canine liver, ear and scrotal skin and rat tongue, no such cells were found in any species (except the cow) in any part of the vascular wall. The results indicate that in most species histamine is stored in the vascular wall in a non-mast cell pool which may well be in the smooth muscle cells themselves.
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PMID:Evidence for non-mast cell histamine in the vascular wall. 116 63

Human mast cells were obtained from adenoids and mesentery by enzymatic dispersion of the tissues with the enzyme collagenase. The digestion of the tissues resulted in a cell suspension which contained 1-2% mast cells. 37.3% (adenoids) and 33.4% (mesentery) of total histamine initially present in the tissues was recovered in the dispersed cell suspensions. More than 90% of the cells were viable. The adenoidal mast cells could be sensitized passively in vitro with homologous reaginic serum and released histamine after challenge with specific antigen. Both populations of mast cells were sensitive to the action of anti-human IgE; the reversed anaphylaxis with anti-IgE was higher in mesenteric mast cells. Both examined mast cell populations were sensitive to the challenge with polymyxin B, concanavalin A and ionophore A23187, however, histamine release was only up to 10% and 20% for adenoidal and mesenteric cells, respectively. Only mesenteric mast cells responded to the action of compound 48/80. Histamine release, induced by polymyxin B, was rapid (maximal release within 5 min), maximal in the presence of 3 mM extracellular calcium ions (but also occurred in the absence of the cation).
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PMID:Histamine secretion from human mesenteric and adenoidal mast cells. 128 67

The regulation of histamine release from oxyntic mucosa is complex because of two potential sources of histamine: mast cells and enterochromaffin-like (ECL) cells. A gastrin-responsive histamine pool was identified in the rat oxyntic mucosa two decades ago, but these ECL cells from the rat have not yet been isolated or characterized in vitro. In vivo studies in canine and human mucosa have been more difficult because of the high content of histamine in mast cells. Using enzyme-dispersed canine oxyntic mucosal cells, we have studied regulation of histamine release from a mast cell-depleted fraction prepared by sequential elutriation and density gradient. Histamine-like immunoreactivity was demonstrated, using peroxidase-anti-peroxidase immunohistochemistry. After short-term culture, histamine was released in response to gastrin, cholecystokinin, carbachol, and forskolin. Somatostatin potently and effectively inhibited the response to gastrin. The cultures used for these studies also contained somatostatin cells, and, furthermore, the response to gastrin was enhanced by incubation with monoclonal antibodies to somatostatin. The latter findings suggested that somatostatin was acting in these cultures by a paracrine route. This pattern contrasts with that obtained in previous studies of canine oxyntic mucosal mast cells.
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PMID:Regulation of histamine release from oxyntic mucosa. 128 99

Agents derived from mast cell granule constituents, and compound 48/80 which stimulates release of mast cell granules, have been used by us to develop new methods for quantitating angiogenesis in the chick chorioallantoic membrane. Two of these methods provide different insights, demonstrating different patterns of response to dosage and over time, produced by different agents. Counting mesenchymal blood vessels is convenient for obtaining dose-response data. Histamine and compound 48/80 have been shown previously to give a sigmoid dose-response curve resulting in a plateau before the lethal dose. This contrasts with the effect of porcine sodium heparin (Evans Biologicals) which results in a minor increase then a relative decline in vessel number due to a failure of growth. Here, the ability to produce angiogenesis or antiangiogenesis appears to be dose-dependent. Measurement of the changes in DNA synthesis, leading to visible angiogenesis, may be performed once the optimal angiogenic dose is known, and again distinctive patterns of response with different agents have been found. Histamine results in a fall then rise to a peak at 36 hr. We now show that two types of heparin each produce a peak at 12 hr. Compound 48/80 results in a distinctive pattern that looks like a composite of the histamine and especially the heparin effects, and this suggests that both are relevant to induction of angiogenesis by mast cells. The elicitation of this pattern of response also provides a method, additional to electron microscopy, for discovering whether or not an angiogenic substance is likely to operate via mast cell stimulation. Such characteristic patterns offer a new way of classifying angiogenic substances.
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PMID:Patterns of angiogenic response to mast cell granule constituents. 137 83

Incubation of either C3a, C3ades Arg, or synthetic analogues of the C-terminal sequence of C3a with purified rat peritoneal mast cells resulted in a rapid and dose-dependent histamine release. The natural factors C3a and C3ades Arg were the most active of the factors tested exhibiting EC50 values of 3.3 and 2.2 microM, respectively. The corresponding 21- and 22-residue C-terminal analogues of C3a (Y21R and Y21) were less potent than intact factor exhibiting EC50 values of 10.9 and 25.1 microM, respectively. Histamine was released in a nonlytic manner and the mast cell stimulation by both natural and synthetic factors was sensitive to pertussis toxin, neuraminidase, benzalkonium chloride, and to an excess of calcium. C3a stimulated the generation of inositol polyphosphates that was inhibited by either pertussis toxin or benzalkonium chloride. The C3a anaphylatoxin also directly stimulates purified G proteins (i.e., GTPase activity) in a dose-dependent manner. The evident correlation between efficiency of C3a and C3a analogues to stimulate purified G proteins and their capacity to induce cellular histamine release led us to conclude that C3a fails to activate mast cells via a mechanism involving specific receptors on the cell. Instead, we propose that C3a either causes direct activation of G proteins of the Gi subtype, with a subsequent activation of phospholipase C, or interacts with a binding site of the cell surface specific for cationic molecules that is coupled to the G protein cascade.
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PMID:A mechanism of action for anaphylatoxin C3a stimulation of mast cells. 137 70

Impaired metabolism of histamine in the skin of patients with chronic idiopathic urticaria (CIU) might explain the observed enhanced and prolonged skin responses to intradermal histamine. Histamine metabolism was measured in homogenates from unaffected forearm skin in nine patients with CIU and in skin of age- and sex-matched control subjects with a radiochromatographic assay, and the results are expressed as nanograms of histamine metabolized per milligram of protein per hour. Endogenous histamine content was determined by RIA. There was a highly significant increase in endogenous histamine content in the skin of patients with urticaria (407.8 +/- 188.3 ng/mg of protein) compared with that in skin of control subjects (240.0 +/- 73.0 ng/mg of protein) (mean +/- 1 SD; p less than 0.02), which suggests either an increase in mast cell number or histamine concentration per cell. No significant difference was observed in the metabolism of histamine between patient and control group; therefore, an alternative mechanism may underlie differences in skin reactivity to histamine.
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PMID:Cutaneous histamine metabolism in chronic urticaria. 137 71

A simple method is described for the preparation of large numbers of mast cells from mouse spleen cells in vitro. Mouse spleen cells were cultured with RPMI 1640 medium supplemented with 10% FCS and 2-ME. Half of the total volume of the medium was changed every 4-5 days. Mast cell numbers increased with the culture time and reached a peak between 16 and 20 days. Using this method, 2 x 10(6) mast cells could be induced from 1 x 10(7) nucleated normal spleen cells. T cells and supernatant derived from ConA-stimulated T cells were unnecessary for mast cell induction. Phenotype analysis by FACS showed that Thy1,2, L3T4, Ly-2, Ig, B220, Asialo GM1, and WGA receptors were all negative but functional IgE receptors were positive. The granules in the cells could be stained by alcian blue but not by safranin. There was 1.632 +/- 0.024 micrograms stored histamine in 1 x 10(6) of the cells. Histamine was released from the cells in an antigen-induced and IgE-mediated process. Compound 48/80 and A23187 induced degranulation of the cells, and the mast cells were able to respond to ConA.
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PMID:Induction and identification of mast cells from long-term culture of mouse spleen cells without conditioned medium. 137 14


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