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)

1. Guinea pig parenchymal lung strips and tracheal smooth muscle contract potently after NaF-addition. Maximal contractions of lung strips and tracheal rings induced by NaF were 208 +/- 17% (n = 6) and 151 +/- 8% (n = 4) of the maximal histamine response respectively. 2. The -log EC50-value for NaF on lung strips and tracheal rings was 2.38 +/- 0.01 (n = 6) and 2.28 +/- 0.01 (n = 4) respectively. 3. Contractions induced by NaF were augmented after Al3+ pretreatment, suggesting the involvement of a G-protein. NaF responses were not affected by blockade of H1-, muscarinic-, leukotriene C4- or leukotriene D4-receptors, indicating that mast cell degranulation or nerve activation is most probably not implicated. 4. Contractions after NaF-addition were relatively insensitive to removal of extracellular calcium and were reversed via cAMP- and cGMP-mediated pathways. 5. Relaxation studies with (-)isoprenaline and 8-bromo-cGMP on lung strips, precontracted to similar levels with either a H1-agonist, KCl or NaF, showed that the level of relaxation depends on the contractile agent that is used. 6. After precontraction with KCl (-)isoprenaline relaxes lung strips only to 58 +/- 9% (n = 5) of the initial contraction, whereas lung strips precontracted with NaF or a H1-agonist relax 114 +/- 8% (n = 4) and 120 +/- 7% (n = 5) respectively with (-)isoprenaline. 7. Similar results were obtained with relaxation induced with 8-bromo-cGMP. 8. These findings suggest that NaF-induced contractions are elicited via a mechanism, that is probably similar to that of the H1-receptor. The involvement of a G-protein in the observed NaF-responses is therefore likely.
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PMID:Fluoride is a contractile agent of guinea pig airway smooth muscle. 165 87

Rat serosal mast cells were evaluated for their capacity to generate a nitric oxide-like factor by two bioassays: inhibition of platelet aggregation and stimulation of mast cell guanylate cyclase. Incubation of mast cells with human washed platelets, both treated with indomethacin, inhibited thrombin-induced platelet aggregation which was potentiated by superoxide dismutase and reversed by oxyhaemoglobin. When mast cells alone were stirred at 1000 rpm, a time dependent increase in the levels of their cGMP but not cAMP was observed. Preincubation of mast cells with NG-monomethyl-L-arginine significantly enhanced E. coli lipopolysaccharide-evoked histamine release. Our results show that mast cell histamine release can be modulated by an intrinsically generated nitric oxide-like factor.
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PMID:Rat mast cells synthesize a nitric oxide like-factor which modulates the release of histamine. 171 38

Rat serosal mast cells were tested for their ability to generate a nitric oxide-like factor by two bioassay systems: inhibition of platelet aggregation and stimulation of mast cell guanylate cyclase. Incubation of rat serosal mast cells with human washed platelets resulted in an inhibition of thrombin-induced platelet aggregation proportional to the number of cells. The inhibition was potentiated by superoxide dismutase (SOD) and reversed by oxyhaemoglobin (oxyHb). The inhibitory activity of mast cells was also prevented by NG-monomethyl-L-arginine (MeArg), an effect reversed by co-incubation with L-Arg but not D-Arg. When mast cells alone were stirred at 1,000 rpm, a time-dependent increase in the levels of their cGMP but not cAMP was observed. This increase was reduced by pretreatment with MeArg. The inhibitory effect of MeArg was reversed by L-Arg but not D-Arg. These results demonstrate that rat mast cells release a factor with the same pharmacological profile as NO, and that this NO-like factor is derived from L-arginine.
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PMID:Synthesis of a nitric oxide-like factor from L-arginine by rat serosal mast cells: stimulation of guanylate cyclase and inhibition of platelet aggregation. 197 20

A significant number of asthmatic subjects are provoked by allergic reactions. The underlying pathophysiologic event is mast cell degranulation with the release and generation of the mediators of anaphylaxis. Histamine, one of the major mast cell mediators, causes 10- to 50-fold increases in guinea pig lung cyclic 3',5'-guanosine monophosphate (cyclic GMP) through H1 receptor stimulation. Employing monoclonal antibodies directed at cyclic GMP, immunocytochemical techniques were used to identify those specific cells in lung responding to histamine stimulation with increases in cyclic GMP. The most responsive cells were alveolar and parenchymal macrophages, pleural lining cells, and endothelial and epithelial cells. Little or no increases in bronchial or vascular smooth muscle cyclic GMP was noted. At the height of the reaction, a generalized increase in cyclic GMP staining of all alveolar cells was observed. These findings suggest that the lining cells of the lung including macrophages, mesothelial, endothelial, and epithelial cells may be the most responsive cells to histamine released during allergic responses. The absence of muscular staining suggests that cyclic GMP does not participate in histamine-stimulated muscle contraction.
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PMID:Immunohistochemical localization of histamine-stimulated increases in cyclic GMP in guinea pig lung. 243 77

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

The mast cell mediator, histamine, induces a rapid and transient increase in chloride secretion across monolayers of the human colonic epithelial cell line, T84. Threshold stimulation occurred at 3 X 10(-6) M histamine and a maximal effect at 10(-4) M. The effect was reproduced by the H1 agonists 2-methylhistamine and 2-pyridylethylamine, but not by the H2 agonists 4-methylhistamine and dimaprit, suggesting the involvement of an H1 receptor. Additionally, histamine's action was inhibited by an H1 antagonist, diphenhydramine, but not by an H2 antagonist, cimetidine. Histamine treatment increased free cytosolic calcium levels, but not those of adenosine 3',5'-cyclic monophosphate (cAMP) or guanosine 3',5'-cyclic monophosphate (cGMP). The mechanism of chloride secretion induced by histamine resembled that of carbachol, in that both 1) were associated with an increase in free cytosolic calcium, 2) had a site of activation at a basolaterally localized K+ channel, and 3) were potentiated by both cAMP- and cGMP-mediated secretagogues. These results suggest that histamine may act as an intestinal secretagogue via direct interactions with epithelial cells.
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PMID:Immune-related intestinal Cl- secretion. I. Effect of histamine on the T84 cell line. 333 21

Theophylline (2.5 mM) did not influence the spontaneous release of histamine but inhibited histamine release induced by antigen, compound 48/80 or phosphatidylserine. The effect on 48/80-induced histamine release could not be reversed by increasing extracellular Ca2+. Exogenous adenosine (10(-8) to 10(-4) M) did not influence spontaneous histamine release or 48/80-induced release but potentiated antigen-induced release. The adenosine potentiation was competitively inhibited by theophylline in concentrations (10(-5) to 10(-4) M) lower than those required to inhibit antigen-induced histamine release in the absence of adenosine. In order to see if endogenous adenosine levels are high enough to potentiate an anaphylactic histamine release in vivo, adenosine was determined in mast cell incubates and in plasma from 4 different strains of rat. The levels were 0.18 to 0.99 microM in plasma, which is sufficient to cause significant potentiation of histamine release, but only 3 x 10(-8) M in mast cell incubates. Theophylline (2.5 mM) increased cAMP levels about 100%, whereas adenosine (10(-5) M) had little effect on cAMP and cGMP levels. However, when incubated together, adenosine could inhibit the theophylline-induced increase in cAMP levels but not the inhibition of histamine release. It is concluded that the effect of low concentrations of theophylline could be due partly to antagonism of adenosine effects. In addition, in higher doses, theophylline appears to exert an inhibitory action that is unrelated to cyclic nucleotides, extracellular calcium and adenosine.
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PMID:On the mechanism by which theophylline inhibits histamine release from rat mast cells. 618 49

Challenge of rat peritoneal mast cells with anti-rat IgE induces a similar pattern of protein phosphorylation to that already reported for compound 48/80. Rapid phosphorylation of a mast cell protein, mol. wt 78,000, is induced by sodium cromoglycate and several chemically related anti-allergic agents in the absence of any challenge. Phosphorylation of this protein reflects their potency in inhibiting anti-IgE-induced histamine release. Compounds which inhibit histamine release by elevating intracellular cAMP levels do not induce phosphorylation. However, dibutyryl-cGMP induces phosphorylation of the 78,000 mol. wt protein in the absence of any challenge, at concns which inhibit IgE-dependent histamine release. Sodium cromoglycate appears to activate an endogenous control mechanism for switching off mediator release using a mechanism mediated by cGMP.
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PMID:Phosphorylation of a mast cell protein in response to treatment with anti-allergic compounds. Implications for the mode of action of sodium cromoglycate. 640 82

The anaphylactic function of IgE has been intensively investigated. The Fc epsilon receptor on mast cells or basophils combines with the last two constant domains of the epsilon heavy chain. The Fc epsilon receptor is apparently a glycoprotein, monovalent and free in the plasma membrane. The interaction between the antigen (allergen) and the corresponding IgE antibody combined with the Fc epsilon receptor results in the aggregation of the receptors. Receptor dimerization suffices to trigger the cell. Compartments can be described in mast cells or basophils, the activity of which depends upon the number of formed receptor dimers on the corresponding membrane area. Beyond a threshold number of dimerized receptors, the cell compartment is triggered, which in the presence of Ca++ leads to the discharge of mast cell mediators, an increasing function of the dimer number. Excess receptor aggregation or the absence of aggregation (i.e. IgE-Ag2 complexes) deactivates the cell, which occurs more often in the absence of Ca++. Thus, IgE molecules play a passive role only in allowing the aggregation of the receptors which delivers the activating signal. But through the composition of IgE-antigen complexes bound to the receptors, IgE also modulates the cell function according two antagonistic reactions in permanent balance, i.e. activation or deactivation. IgE molecules are also involved in immediate type reactions in inducing the release of lysosomal enzymes from mononuclear phagocytes. But IgE antibody can also, when complexed with the antigen, trigger macrophage cytotoxicity for the corresponding target, which indicates a new function of IgE in the effector mechanisms of immunity of particular importance in immunity to schistosomes. A receptor for aggregated IgE has been characterized on the membrane of macrophages. The binding of IgE to its macrophage receptor triggers the cell, as shown by the resulting increase in cyclic GMP, calcium uptake and accelerated turn-over of lysosomal enzymes. A receptor for IgE has also been described on lymphoid cells, B cells, null cells and recently T cells, and the appearance of the receptor is modulated by IgE molecules themselves, suggesting a homeostatic role of IgE molecules. IgE appears thus to play various functions, the most dramatic being the triggering of anaphylactic reactions. But the role of IgE in activating mononuclear phagocytes or lymphoid cells might also prove to be of importance in immunity.
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PMID:[Cellular interactions of IgE: towards a new function for IgE]. 700 8

We previously established a system for induction of mucosal-type mast cells from mouse spleen cells by long term culture without exogenous IL-3. FCS was important and was able to be divided into mast cell-inducible and non-mast cell-inducible sera. LPS contaminated in FCS was responsible for the mast cell induction. However, we unexpectedly found that both supernatants recovered from the cultures with mast cell-inducible and non-mast cell-inducible sera contained endogenous IL-3. Furthermore, addition of rIL-3 to the cultures with non-mast cell-inducible sera had no effect or induced only a small number of mast cells. This indicates that IL-3 alone is not enough for mast cell induction and that some inflammatory factor(s) induced by LPS is also essential. Prostaglandin E1 (PGE1) and PGE2 induced mast cells in a dose-dependent manner when added into the cultures. The activity of LPS for mast cell induction was inhibited by indomethacin. However, indomethacin failed to inhibit the mast cell induction by exogenous PGE. Exogenous PGE antagonized the indomethacin-induced inhibition of mast cell induction by LPS. Cholera toxin and dibutyryl cyclic AMP (cAMP) also induced mast cells. The A and B subunits of cholera toxin, PGF2 alpha, PGD2, and dibutyryl cGMP failed to induce mast cells. Furthermore, mast cell induction by PGE was dose-dependently suppressed by inhibitors for cAMP-dependent A kinase. The above results show that for mast cell induction, IL-3 needs the cooperation of PGE or other stimulants that can elevate the production of the second messenger cAMP in mast cell precursors.
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PMID:An essential role of prostaglandin E on mouse mast cell induction. 763 61


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