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)

Pulmonary vasomotor actions of histamine and the possible relationship of histamine to hypoxic pulmonary vasconstriction were studied in anaesthetized cats with one lobe of lung perfused at constant flow and in isolated perfused rat and ferret lungs. In the cat histamine caused dilatation, biphasic responses and constriction with increasing doses. Histamine induced dilatation was better demonstrated during hypoxic vasoconstriction and was reduced by an H2 histamine antagonist; constriction with histamine was abolished by an H1 antagonist. Histamine also caused both vasodilatation and vasoconstriction in ferret lungs. A mast cell stabilizing agent had no effect on hypoxic pulmonary vasoconstriction in cats or rats. This response was unaffected in cats but greatly reduced in rats and ferrets by cyproheptadine, a combined histamine and 5-hydroxy-tryptamine inhibitor. It was unaffected in cats but abolished in ferrets an H1 histamine inhibitor. It was again unaffected in cats but greatly reduced in rats and ferrets by an H2 histamine inhibitor. These species differences may reflect differences in mechanism but more probably reflect non-specific effects of the inhibitors in certain circumstances. However, when drugs nearly abolished hypoxic vasoconstriction, ATP still caused vasoconstriction.
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PMID:H1 and H2 histamine actions on lung vessels; their relevance to hypoxic vasoconstriction. 24 33

The mast cell population is heterogeneous concerning its amine precursor and amine uptake. The immature cells incorporate amine precursors, but in more advanced stages of their maturation they take up only 5-HTP. The mature cells do not take up precursors only 5-HT. The thyroid gland and heart muscle mast cells take up the highest amount of 5-HT; this may be related with some specific function of the mast cells in these two organs. Neither of the mast cells would take up histamine, the compound is synthetised by the cells.
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PMID:Biogenic amine and amine precursor uptake by mast cells. 30 84

The rat mast cell granule chymotrypsinlike enzyme was purified to homogeneity from 1 M NaCl solubilized membrane and granule-rich fractions of concentrated rat peritoneal mast cells by a preparative technique utilizing chromatography on Dowex 1, filtration on Sephadex G-75, and affinity chromatography with D-tryptophan methyl ester. Acid disk gel electrophoresis of the purified chymase disclosed a single stained band with activity being eluted from a replicate sliced gel in the same region. SDS-polyacrylamide gel electrophoresis of purified protein gave a single stained band that did not change in position with reduction and alkylation. Mast cell chymase is thus a cationic protein of 25,000 mol wt composed of a single polypeptide chain. The apparent K(m) of the chymase for BTEE was 1.5 x 10(-3) M and the V(max) was 67.8 mumol/min per mg. The enzyme was inhibited by TPCK and not by TLCK. The chymase complexed with native macromolecular rat mast cell heparin in molar ratios of 12:1 and 16:1, and complete heparin uptake occurred at a 40:1 ratio of chymase to heparin. Chymase activity was partially masked by combination with heparin in the isolated granule or experimental chymase-heparin complex, and soluble purified chymase was inhibited by concentrations of 5-HT comparable to those present in mast cells. It is therefore possible that the active site of chymase in the mast cell granule is largely masked by the combined effects of macromolecular heparin and 5-HT.
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PMID:Preparative purification of the rat mast cell chymase: characterization and interaction with granule components. 33 34

A chronobiologic transverse study on rat thyroid has been carried out to investigate whether mast cells and their content in biogenic amines normally undergo daily variations and whether these are related to circadian activity of the gland. The mean number of mast cells per microscopic field presents daily variations ranging from 10.9 +/- 3 to 14.6 +/- 3.8 in males and from 8.4 +/- 1.9 to 14.8 +/- 3 in females: these variations show a circadian trend in both sexes, with a 12 hrs period and two peaks at about 11:10/23:10. The mean percentage of degranulated mast cells per microscopic fields shows daily variations ranging from 51 +/- 11 to 60.4 +/- 14.2 in males and from 49.8 +/- 12.5 to 58.3 +/- 13.6 in females; these variations present a circadian rhythm with a 24 hrs period and a mean peak at 02:00. The histamine content of the gland varies in 24 hrs from 20.93 +/- 1.19 micrograms/g w w to 38.08 +/- 1.7 micrograms/g w w, without any sex-related difference: these variations show a rhythmic trend with a 12 hrs period and two peaks at 09:10/21:10. Serotonin content of thyroid presents circadian variations from 15.98 +/- 0.83 to 23.23 +/- 0.61 micrograms/g w w, with a 12 hrs period and two peaks at 04:20/16:20. Whereas the variations of mast cell exocytosis and of serotonin content seem to be chronobiologically linked to circadian variations of gland activity, evaluated on the basis of free and total tetraiodothyronine serum levels, the variations of mast cell number appear to be related to those of thyroid and blood histamine. The present data support the hypothesis that mast cell activity should not be considered as only linked to inflammation or allergic responses.
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PMID:Role of mast cells in health: daily rhythmic variations in their number, exocytotic activity, histamine and serotonin content in the rat thyroid gland. 128 37

Three agents known to induce release of mast cell constituents, viz. polymyxin, compound 48/80 and polysorbate-80, were evaluated for effect on perfused blood vessels of R. tigrina and B. melanostictus. The mast cell degranulators caused vasoconstriction in frog and toad, except that for P-80 whose responses in toad were equivocal. Toads showed a general low responsiveness in comparison to frogs. Pharmacologic intervention with pheniramine, metergoline, hydergine, atropine and mecamylamine, respectively ruled out role of histamine, 5-HT, catecholamine or acetylcholine or even autonomic mechanisms in the above phenomena. The observations are suggestive of phylogenetic differences in biochemical profile of mast cells in amphibian species.
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PMID:Comparative effects of mast cell degranulators on perfused systemic blood vessels of Bufo melanostictus and Rana tigrina. 133 98

Staphylococcal enterotoxin B (SEB) was tested in rodent mast cell cultures for the release of serotonin. Both rat RBL-2H3 mast cells and murine peritoneal cells released serotonin after SEB stimulation in culture. Release of serotonin in RBL-2H3 cells depended on the concentration of SEB; an appreciable release was seen at 50 micrograms/ml. The release of serotonin was not due to cell death. Serotonin release could be enhanced by bradykinin but not by vasoactive intestinal peptide, substance P, lipopolysaccharide from Salmonella typhimurium, the calcium ionophore A23187, acetylcholine, adenosine, 5-hydroxyeicosatetraenoic acid, indomethacin, or phorbol myristate acetate. SEB bound directly to the membrane of RBL-2H3 mast cells, and the SEB-binding site, the presumptive receptor, appeared to be a protein. The SEB receptor could not be capped under membrane-capping conditions, and serotonin release could not be enhanced by attempts to cross-link the receptor. These results suggest that mast cells may be an important cell type involved in SEB toxicosis and that release of serotonin may be enhanced by activation of the kinin-kallikrein system.
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PMID:Effects of staphylococcal enterotoxin B on rodent mast cells. 137 85

Neurogenic inflammation has been proposed as a possible pathogenetic mechanism for migraine and cluster headache. Antidromic stimulation of trigeminal fibers causes plasma protein extravasation, mast cell activation and degranulation, vacuolation and increase in endothelial vesicle number within post capillary venules in rat dura mater. The antimigraine drugs sumatriptan and dihydroergotamine block the development of plasma extravasation and ultrastructural changes, as well as plasma calcitonin gene-related peptide (CGRP) increase in the superior sagittal sinus following electrical trigeminal ganglion stimulation. Sumatriptan and dihydroergotamine bind with high affinity to the 5-HT1D/1B receptors, thus suggesting that their neurogenic antiinflammatory activity is mediated by activation of 5-HT autoreceptors present on sensory fibers innervating blood vessels in dura mater.
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PMID:The trigemino-vascular system and migraine. 137 7

Mast cells secrete many biologically active compounds upon stimulation by immunoglobulin E (IgE) and specific antigen (Ag), anaphylatoxins, as well as a number of cationic compounds which include drugs, kinins and neuropeptides. The effects of the two naturally occurring polyamines, spermine (SP) and spermidine (SPD), on mast cell secretion were studied because they have been implicated in the modulation of cellular processes, possibly through their cationic charge or the regulation of calcium ions. SP and SPD over the range of 10(-7) to 10(-4) M inhibited the release of 5-hydroxytryptamine (5-HT, serotonin) triggered by compound 48/80 (C48/80) in a time- and concentration-dependent manner, as long as at least 2% calf serum (CS) was present. SP also inhibited secretion of both histamine and serotonin stimulated immunologically by using IgE and anti-rat IgE. This inhibition was not accompanied by cytotoxicity. The major available polyamine metabolites tested, N1-acetyl spermine (N1-acSP) and N8-acetyl spermidine (N8-acSPD), also showed inhibition in the presence of CS, whereas putrescine, N8,N1-hexamethylene-bis-acetamide (HMBA) and benzylamine did not. Fetal bovine serum (FBS), as well as human and rat serum, which do not contain polyamine oxidase, did not result in any inhibition with the polyamines tested. Inhibitors of the polyamine oxidase blocked the polyamine effect, indicating that the inhibition of mast cell secretion must derive from aldehydes produced from these polyamines. Addition of the aldehyde inhibitor phenylhydrazine (phi-HDZ), simultaneously with, but not following the polyamines, blocked their inhibitory effect, further strengthening the involvement of aldehydes. These results indicate that naturally occurring polyamines may regulate mast cell secretion through metabolic products of polyamine oxidase, a similar enzyme of which is also present in human liver, placenta and pregnant serum.
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PMID:Inhibition of mast cell secretion by oxidation products of natural polyamines. 159 9

SK&F 101926, a synthetic peptide, is a potent antagonist of vasopressin at both the V2 and the V1 receptors. Following intravenous administration of SK&F 101926 (5 mg/kg), mean arterial pressure (MAP) immediately fell 75 mm Hg. Heart rate increased approximately 50 beats/min. Cutaneous flushing and cyanosis appeared approximately 2 to 5 min after the SK&F 101926 administration. Three of the five rats died within 40 min with no improvement in either color or MAP. The two surviving animals slowly recovered from these symptoms. The hypotension and flushing recorded in these studies resembled the effects during hypotensive shock. SK&F 101926 degranulated rat peritoneal mast cells in vitro as measured by the liberation of histamine. Analogs of SK&F 101926 were identified having reduced activity to release histamine from mast cells in vitro. The activity of these analogs to release histamine in vivo was also tested, as reflected by rat paw edema. A positive correlation was found between the potency to produce edema in vivo and the potency to release mast cell histamine in vitro (r = 0.94, p less than 0.05). In addition, compounds that released mast cell histamine and induced rat paw edema also produced hypotension and death when administered intravenously, while analogs which produced minimal histamine release in vitro produced minimal or no cardiovascular changes or lethality in vivo at the same dosages (5 mg/kg). Finally, cyproheptadine (10 mg/kg), an antagonist at both the serotonin and the histamine receptors, blunted the effects of SK&F 101926 on MAP and blocked the lethality. Pretreatment with a combination of histamine (H1 and H2) antagonists provided little protection against the SK&F 101926-induced toxicity. These data indicate that the cardiovascular toxicity of SK&F 101926 (and related peptides) is mediated via the release of autocoids from mast cells. Serotonin appears to play a major role in mediating the cardiovascular toxicity of SK&F 101926.
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PMID:Hypotension induced by vasopressin antagonists in rats: role of mast cell degranulation. 168 65

Addition of the protein synthesis inhibitor cycloheximide (CX, 1 microgram/ml) and the RNA synthesis inhibitor actinomycin D (AD, 0.1 microgram/ml) to unfractionated mouse peritoneal mast cells simultaneously with IgE anti-DNP, for 24 h prior to challenge, completely blocked antigen-induced 5-HT release. Responses to anti-IgE were strongly abrogated whereas responses to the calcium ionophore A23187 were not affected. When CX and AD were added to presensitized cells their effects on antigen and anti-IgE-induced release were much reduced. These results suggest a requirement for protein synthesis during mast cell sensitization.
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PMID:Inhibitors of protein and RNA synthesis block the sensitization of murine peritoneal mast cells. 171


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