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.
Gen Pharmacol 1991
PMID:Fluoride is a contractile agent of guinea pig airway smooth muscle. 165 87

Exogenous addition of purified chymase, a rat serosal mast cell (RSMC) chymotryptic enzyme, results in RSMC degranulation at 37 degrees, but not at 1 degree. Chymase can cause an active site-dependent inducing event at 1 degree such that RSMC degranulation occurs if the cells are later incubated at 37 degrees. RSMC exposed to chymase or other stimuli were surface radiolabelled using 125I and Iodo-Gen, solubilized with 1% Nonidet-40, and the resulting 25,000 g supernatants analysed by SDS-PAGE and autoradiography. A 125I-labelled RSMC membrane protein of approximate 90,000 MW decreased upon exposure to either chymase or alpha-chymotrypsin (alpha-CT) for 5 min at 37 degrees or to chymase for 60 min at 1 degree. Exposure of RSMC to the secretagogues ionophore A23187, compound 48/80, and anti-IgE for 5 min at 37 degrees resulted in beta-hexosaminidase (a secretory granule enzyme) release, but did not cause a detectable change in the 90,000 MW surface-labelled protein. Lima bean trypsin inhibitor, which inhibits both the esterase and RSMC degranulation activities of chymase and alpha-CT, prevented the disappearance of the 125I-labelled 90,000 MW band when added with chymase or alpha-CT. Exposure of RSMC to chymase at 1 degree for 0-10 min, prior to addition of LBTI, led to a progressive disappearance of the 90,000 MW band, which corresponded to the kinetics of priming for subsequent RSMC degranulation at 37 degrees. When RSMC were exposed to trypsin (2.5 micrograms/ml) for 0-120 min at 1 degree, a progressive disappearance of the 90,000 MW band occurred, in association with a loss of sensitivity to subsequent activation by chymase at 37 degrees. The disappearance of the 90,000 MW determinant in association with chymase-mediated priming for degranulation and the inability of chymase to mediate degranulation of trypsin-treated RSMC, which lack this membrane protein, suggests that it is involved in chymase-mediated RSMC degranulation.
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PMID:Cleavage of a rat serosal mast cell membrane component during degranulation mediated by chymase, a secretory granule protease. 231 65

We have used the whole-cell patch-pipette technique to measure the step increases in the cell membrane capacitance (equivalent to the membrane area) caused by the fusion of secretory granules in degranulating murine mast cells. We have observed that up to 30% of the total membrane expansion caused by degranulation results from large fusion events that cannot be explained by the fusion of single secretory granules. These large events are observed mainly in the initial phase of a degranulation. We have developed a simple mathematical model for a mast cell to test whether these large events are caused by a stimulus-induced, granule-to-granule fusion that occurs before their exocytosis (multigranular exocytosis). Our results suggest that the large fusion events are caused by the exocytosis of granule aggregates that existed before stimulation and that are located at the cell's periphery. We propose a novel mechanism by which granule aggregates can be formed at the periphery of the cell. This mechanism relies on the ability of a transiently fused granule ("flicker") to fuse with more internally located granules in a sequential manner. This pattern may result in the formation of larger peripheral granules that later on can fuse with the membrane. The formation of peripheral granule aggregates may potentiate a subsequent secretory response.
J Gen Physiol 1990 Mar
PMID:Compound versus multigranular exocytosis in peritoneal mast cells. 232 1

Lidocaine, W49091, procaine and benzocaine inhibited mast cell secretion induced by concanavalin A and A23187. They inhibited Ca influx stimulated by concanavalin A, suggesting that they inactivate Ca channel of mast cells. Lidocaine and procaine inhibited Ca influx stimulated by A23187, but W49091 and benzocaine did not.
Gen Pharmacol 1985
PMID:Different effects of local anesthetics on calcium influx into rat mast cells. 241 Mar 24

(-)3-[125I]iodocyanopindolol (ICYP), a high selective, high specific beta antagonist is employed to characterize beta-adrenoceptors on rat pleural and peritoneal mast cell populations. Results show that non specific binding is low, and that pleural mast cells exhibit greater number of receptors per cell (140,000) than peritoneal cells (90,000). Dissociation constants (Kd) are 0.37 +/- 0.01 and 0.55 +/- 0.02 nM for pleural and peritoneal cells, respectively. Competition experiments show that isoproterenol do not displaces ICYP neither in pleural nor in peritoneal cells. Low concentrations of propranolol displace ICYP from its binding sites, but atenolol does not. Results point to the existence in mast cells of mainly atypical. beta 2-receptors, since the agonist isoproterenol does not compete with the antagonist ICYP.
Gen Pharmacol 1987
PMID:Adrenergic agonists do not compete with the antagonist (-)3-[125I]iodocyanopindolol for binding to rat pleural or peritoneal mast cell adrenergic receptor. 288 71

Twenty-one-day-old rats were treated with mast cell stimulators or inhibitors. Mast cell inhibition produced decrease of total cholesterol in plasma and aorta, while the stimulation led to an increase. Both stimulation and inhibition produced increased levels of plasma and aorta triglycerides, and decrease of aorta content of hexosamine, hydroxyproline and total protein; these same effects could be due to different release of specific mast cell mediators.
Gen Pharmacol 1986
PMID:Effect of mast cell stimulators or inhibitors on plasma lipids and aortic content of lipids, hexosamine and hydroxyproline in rats. 308 3

Twenty-one-day-old rats were treated with mast cell inhibitors for four weeks. Some of the rats were thyroidectomized in the beginning of the experiment. Mast cell impairment decreased plasma cholesterol and increased plasma triglyceride levels; in aorta, there was a decrease in total protein, hexosamine and hydroxyproline levels, while triglyceride concentration increased and total cholesterol did not change. In thyroidectomized rats, mast cell impairment led to decreased plasma cholesterol and aortic triglyceride content, increased aortic hexosamine and hydroxyproline levels and did not change plasma triglycerides, aortic total cholesterol and total protein content. It was concluded that some effects of mast cell inhibition on arterial wall metabolism are mediated through the thyroid gland.
Gen Pharmacol 1986
PMID:Effects of mast cell inhibition on plasma and aortic content of lipids, hexosamine, and hydroxyproline in rats. Role of thyroid gland. 308 33

We used the mast cell as a model system for studying some of the membrane events which occur during exocytosis. Our observations indicate that the maximum cluster size of IgE molecules necessary for the "on" signal to activate a mast cell is 10 or less and that the "off" signal is not associated with the gross patching or pinocytosis of IgE and its Fc receptors. Furthermore, the use of Con A-Sepharose beads to stimulate mast cells has shown that such signaling is localized to the areas of stimulus, but this localization is not a function of desensitization over the rest of the cell since the subsequent addition of soluble Con A to locally released cells induced generalized degranulation. Ca2+ influx therefore acts in a localized manner to initiate degranulation. Following receptor cross-linking, most of the membrane proteins and the layer of intervening cytoplasm are laterally displaced away from the areas of membrane interaction. This displacement may act as the signal for fusion to occur. The resulting fused bilayers are predominantly lipid, a situation which may be common in all transient membrane fusion. The mechanism of exposing histamine-containing granules to the extracellular space by blebbing is discussed.
Soc Gen Physiol Ser 1980
PMID:Rat peritoneal mast cells: a model system for studying membrane fusion. 624 65

Multiple forms of urotensin II (UII), one of the hormonal peptides of the caudal neurosecretory system of fishes, were purified from the urophyses of the carp, Cyprinus carpio. Three distinct peaks with UII activity (classified as UII-alpha, -beta and -gamma) were separated by reverse-phase high-pressure liquid chromatography (HPLC). Edman degradation as well as digestion with carboxypeptidase A revealed the primary structures of these peptides as UII-alpha: Gly-Gly-Gly-Ala-Asp-Cys-Phe-Trp-Lys-Tyr-Cys-Val UII-beta: Gly-Gly-Ser-Asn-Thr-Glu-Cys-Phe-Trp-Lys-Tyr-Cys-Val UII-gamma: Gly-Gly-Gly-Ala-Asp-Cys-Phe-Trp-Lys-Tyr-Cys-Ile The results of thin-layer chromatography, HPLC, amino acid analysis, and sequencing indicate that UII-alpha and -gamma are homogeneous. UII-beta appears, however, to be a mixture of two components, differing only at position 2. Thus, in the carp urophysis, four forms of UII appear to be present, although the separation of two components in UII-beta has not been obtained. Sequence of positions 6-11 is common to all forms of UII isolated from the carp, sucker (Catostomus commersoni) and goby (Gillichthys mirabilis).
Gen Comp Endocrinol 1984 Jul
PMID:Primary structures of multiple forms of urotensin II in the urophysis of the carp, Cyprinus carpio. 674 27

1. Polyethylenimine with a molecular weight of 600 (PEI6) was the simplest and the most useful to investigate mast cell-activating mechanisms via pertussis toxin (IAP)-sensitive G protein pathway. 2. IAP, lidocaine, or dibutyryl cyclic AMP were inhibitors of the histamine release induced by PEI6, but anti-allergic drug DSCG, the calcium antagonist, D-600, kinase inhibitors, H-7 and K252a, or the calmodulin inhibitor, W-7 were not. 3. The additive effects of compound 48/80 and PEI6 suggested that the action sites for PEI6 overlapped the binding sites of compound 48/80. 4. Mast cell activation induced by PEI6 was sugar-specifically inhibited by N-acetylglucosamine(Glc-NAc)-specific lectins and/or by sialic acid (Sia)-specific lectins, suggesting that the action sites for PEI6 were glycoproteins having GlcNAc and/or Sia residues. 5. Four glycoproteins seemed to be involved in histamine release, including the IAP-sensitive G-protein pathway.
Gen Pharmacol 1995 Oct
PMID:PEI6, a new basic secretagogue in rat peritoneal mast cells: characteristics of polyethylenimine PEI6 resemble those of compound 48/80. 759 Jan 4


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