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)

Catalase is a characteristic enzyme of peroxisomes. To study the molecular mechanisms of the biogenesis of peroxisomes and catalase in a less complex system than rat liver cells, we expressed recombinant rat catalase in Escherichia coli, which has no peroxisomes. The concentration of recombinant catalase produced in E. coli transformed with the expression vector carrying the complete coding region of rat catalase cDNA was about 0.1% of the total soluble protein. The recombinant catalase was purified by DEAE-cellulose column chromatography followed by acidic ethanol precipitations. The properties of rat liver catalase and those of the recombinant were similar with respect to molecular mass, catalytic properties, profiles of absorption spectra, and iron contents. The NH2-terminal amino acid sequence of the purified recombinant catalase, as determined by Edman degradation, was in complete agreement with the amino acid sequence predicted from the nucleotide sequence of rat catalase cDNA, except that the first initiator methionine was not detected. The COOH-terminal amino acid sequence was determined by carboxypeptidase A digestion and the sequence, -Ala-Asn-Leu-OH, matched the predicted COOH-terminal amino acid sequence of rat catalase. Recombinant rat catalase gave almost the same multiple protein bands on native polyacrylamide gel isoelectric focusing as observed with authentic rat liver catalase.
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PMID:Purification and properties of recombinant rat catalase produced in Escherichia coli. 220 16

The effects of ethanol and related short-chain alcohols on histamine release from purified rat mast cells were compared to the effects of the alcohols on mast cell membrane properties. Concanavalin A (Con A) (9.3-2790 nM) and somatostatin (0.61-61 microM) stimulated histamine release in a concentration-dependent manner. Ethanol (10-500 mM) had little effect on histamine release itself. However, it inhibited Con A- and somatostatin-stimulated release. Con A was more sensitive to the inhibitory effects of ethanol. For example, 100 mM ethanol inhibited Con A-stimulated release by 56%, whereas somatostatin-stimulated release was reduced only 28%. Mast cell membranes were prepared and the membrane order estimated by determining the fluorescence polarization of diphenylhexatriene. Ethanol (10-500 mM) decreased the fluorescence polarization of mast cell membranes, suggesting a decrease in membrane order. The changes in membrane order by ethanol correlated (r2 = 0.99) with both the inhibition of Con A- and somatostatin-stimulated release. Changes in membrane polarization due to a temperature change from 35 degrees C to 40 degrees C also correlated with changes in receptor-stimulated histamine release. The effects of a series of alcohols related to ethanol on stimulated histamine release and mast cell membrane organization were similar to ethanol and dependent on the lipophilicity of the alcohol. These findings suggest that alcohol effects on membranes can alter receptor function and that certain receptors, e.g., Con A, are more sensitive to the membrane actions of ethanol or related alcohols than are other receptors, e.g., somatostatin.
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PMID:Correlation of ethanol's membrane actions and inhibition of receptor-stimulated histamine release from rat mast cells. 242 70

Prostaglandins have been shown to prevent the damage to the gastric and intestinal mucosa which has been induced by diverse necrotizing substances. These damaging stimuli increase the liberation of histamine from mast cells. Because of its well known effects on cellular permeability, histamine may serve the initial stimulus for mediating cellular damage. The aim of our study was to investigate the effect of misoprostol, a synthetic PGE1 analog, on tissue histamine concentration and mast cell counts after damage to the gastric mucosa induced by stress, histamine, aspirin and concentrated ethanol in guinea pigs. Misoprostol or its matching placebo were administered intragastrically 3 minutes prior to the ulcerogenic stimulus. After the induction of the injury, the animals were sacrificed, stomachs were examined for ulceration. Gastric and duodenal histamine concentrations were determined. Mast cells from these organs were stained and counted. All four ulcerogenic stimuli resulted in significant gastric ulcer formation. This ulcerogenic action was accompanied by a significant decrease in mucosal histamine concentration and mast cell counts. Misoprostol induced a dose-dependent inhibition of gastric damage, histamine depletion and mast cell destruction. These results indicate that the stabilization of mast cells by misoprostol is an important mechanism for its mucosal protective effects against ulcerogens.
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PMID:Misoprostol prevents damage to the gastric mucosa by stabilizing the mast cells. 244 10

The mechanism of action of the "mast cell stabilizers" sodium cromoglycate and FPL-52694 as protective agents against ethanol-induced gastric mucosal damage was investigated in the rat. Using an ex vivo gastric chamber model, various concentrations (10-80 mg/mL) of the two agents were applied to the gastric mucosa prior to exposure to 40% ethanol. Both agents significantly reduced ethanol-induced damage in a dose-dependent manner. When given orally (80 mg/kg) both agents significantly reduced gastric damage induced by subsequent oral administration of absolute ethanol. Pretreatment with indomethacin did not significantly affect the protection afforded by FPL-52694, but did cause a partial reversal of the protective effect of sodium cromoglycate. Changes in gastric leukotriene C4 synthesis did not correlate with the protective effects of the two agents. Both mucosal and connective tissue mast cell numbers were significantly reduced following oral ethanol administration. In the groups pretreated with FPL-52694 or sodium cromoglycate, mucosal mast cell numbers were not significantly different from those in rats not treated with ethanol. Furthermore, the connective tissue mast cell numbers were significantly lower than in ethanol-treated control rats, despite a greater than 95% reduction of ethanol-induced hemorrhagic damage. These results therefore suggest that stimulation of gastric prostaglandin synthesis is not important in the mechanism of action of FPL-52694, and neither agent appears to reduce damage through a mechanism related to effects on gastric leukotriene C4 synthesis. The present studies further suggest that the protection afforded by pretreatment with sodium cromoglycate or FPL-52694 may be unrelated to effects of these agents on the connective tissue mast cell population in the stomach.
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PMID:Reduction of ethanol-induced gastric damage by sodium cromoglycate and FPL-52694. Role of leukotrienes, prostaglandins, and mast cells in the protective mechanism. 250 42

Mast cell heterogeneity has been described on the basis of differential staining reactions, light microscopic morphology, anatomic location, degranulation after polyamines, biochemical contents, growth requirements, and reactions to lymphokines. We have demonstrated typical "connective-tissue mast cells" by using anatomic criteria, histological staining reactions, electron microscopy, and reaction to compound 48/80 in the guinea pig conjunctiva, eyelid skin, and ileum. A second, much larger population of cells in the ileal mucosa and the conjunctiva, and rarely in the eyelid skin stained reddish-blue with acid toluidine blue in tissue fixed in ethanol-acetate-lead subacetate (BLA) and with alkaline Giemsa in formaldehyde-fixed tissue, did not stain with ethanolic or acid toluidine blue in formaldehyde-fixed tissue or with alkaline Giemsa in BLA-fixed tissue, and did not degranulate after 48/80 treatment. These are features of the rat intestinal "mucosal mast cells"; however, ultrastructural and light microscopic studies with the orcein Giemsa stain demonstrated these cells in the guinea pig to be eosinophils. Tissue culture, biochemical, and immunological studies indicate the existence of a second type of mast cell (bone-marrow-derived mast cell), ultrastructurally almost indistinguishable from the connective tissue mast cell. Our studies demonstrate only one mast cell type in the guinea pig and support the contention that other forms of mast cells are immature forms or variants of the connective-tissue mast cell.
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PMID:Eosinophils and mast cell homogeneity of the guinea pig eyelid skin, conjunctiva, and ileum. 258 20

The effect of some gastroprotective agents cysteamine, sodium salicylate, atropine, cimetidine, and pyrido-pyrimidine derivatives, rimazolium, Ch-127 and a mast cell stabilizer, BMY-26517-31 was studied on the enhanced vascular permeability of gastric mucosa induced by 100% ethanol, on the enhanced vascular permeability of peritoneal blood vessels due to 0.3% acetic acid and on carrageenin edema test. We found that cysteamine, sodium salicylate, rimazolium and BMY-26517-31 inhibited the alcohol-induced enhanced vascular permeability. They also decreased the carrageenin-induced edema and--with the exception of BMY-26517-31--the acetic-acid-induced enhanced vascular permeability of the peritoneal vessels. These results suggest that similar events are present in the early phase of acute inflammation and chemically induced mucosal lesions. Consequently, antiinflammatory activity might play role in the protective mechanism of some anti-ulcer agents.
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PMID:The effect of some anti-ulcer agents on the early vascular injury of gastric mucosa induced by ethanol in rats. 259 6

Nine biopsy specimens from the jejunum of patients with a clinical history of food allergy and 10 from the rectal mucosa of patients with presumed 'allergic proctitis' were fixed in cold ethanol and further processed for paraffin embedding. Serial tissue sections were stained for IgE by direct (polyclonal antibody) and indirect (monoclonal antibody) immunofluorescence methods. Adjacent sections were subjected to conventional mast cell staining (astra blue). In all mucosal specimens from the jejunum and in 8 rectal ones, numerous cells were found to be positive both for astra blue by transmission microscopy and for IgE by fluorescence microscopy of the same section. With the monoclonal antibody all astra-blue-positive cells were IgE-positive; however, this was not always the case with the polyclonal reagent, probably because the fluorescence was weaker with the direct technique. Detection of IgE-positive mucosal mast cells may turn out to be of diagnostic interest in patients with adverse reactions to food.
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PMID:IgE-positive cells in human intestinal mucosa are mainly mast cells. 266 1

This study evaluated the effects of topical isoproterenol, a beta-adrenergic agonist, on the morphologic damage produced in the gastric mucosa by ethanol. The orogastric instillation of 100% ethanol in rats resulted in gross lesion formation and deep histologic injury in the gastric mucosa. Animals pretreated with oral isoproterenol (50 micrograms/kg, 500 micrograms/kg, 50 mg/kg) showed dose-dependent protection from both the gross and the histologic mucosal injury (P less than 0.01, ANOVA). Pretreatment with propranolol (2 mg/kg/sec) but not indomethacin (5 mg/kg/sec) blocked this protective effect. Isoproterenol had no effect on ethanol-induced mast cell degranulation as both mucosal and submucosal mast cell counts were significantly and equally decreased in all groups treated with 100% ethanol (P less than 0.05). These findings show that topical isoproterenol protects the rat gastric mucosa from both the gross and the histologic injury caused by 100% ethanol. This protection is mediated by a beta-adrenergic receptor mechanism as it can be blocked by prior treatment with propranolol, but does not involve stabilization of mucosal or submucosal mast cell membranes.
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PMID:Topical isoproterenol protects the rat gastric mucosa from ethanol-induced injury. 273 24

Somatostatin prevents hemorrhagic gastric erosions produced by ethanol. In this paper we describe studies with linear (reduced) and cyclic (oxidized) synthetic somatostatin-14 in the rat model of ethanol-induced gastric mucosal injury. The linear form of somatostatin was more potent at concentrations of 10(-9) to 10(-8) mol per rat than the cyclic isomere. However, at a concentration of 10(-7) mol per rat i.p. injection of linear somatostatin significantly (P less than 0.01) enhanced gastric erosions caused by the alcohol. The area of hemorrhagic mucosal lesions correlated significantly (r = -0.846) with mast cell depletion in the gastric mucosa of the animals. Increased vascular permeability and mast cell degranulation were also observed after intradermal injection of linear or cyclic somatostatin. The 'cytoprotective' as well as the aggravating potency of linear somatostatin may be connected to gastric mucosal mast cell activity in the rat.
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PMID:Dose-dependent effects of linear and cyclic somatostatin on ethanol-induced gastric erosions: the role of mast cells and increased vascular permeability in the rat. 287 90

Somatostatin (S) inhibits hemorrhagic gastric erosions produced by ethanol. In this study we compared the dose-dependent effects of linear (reduced) and cyclic (oxidized) S with respect to mast cell degranulation. The gastric mucosal injuries were more inhibited by linear S than by cyclic S. But linear S aggravated injury at a certain dose (10(-7) mol/rat). Mucosal mast cell degranulation correlated significantly with the area of hemorrhagic mucosal lesions (r = 0.91). Both cytoprotection as well as aggravation potency of S may be connected to gastric mucosal mast cell activity in the rat.
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PMID:Effects of somatostatin on ethanol-induced gastric erosions in the rat: role of mast cells. 287 24


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