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Query: UNIPROT:P15088 (
mast cell
)
14,925
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In the presence of L-cysteine, a selective and marked enhancement of the in vitro, immunologic release of slow reacting substance of anaphylaxis (SRS-A) from human peripheral leukocytes, sensitized monkey lung fragments, and sensitized guinea pig lung fragments was observed. In the rat, cysteine, but not
sodium
sulfide, enhanced the calcium ionophore (A23187)- induced release of SRS-A in vitro from mixed rat peritoneal cells and in vivo from the rat peritoneal cavity. Pretreatment of rats with cysteine also enhanced the IgGa-and anti-rat IgE-mediated release of SRS-A in vivo in the rat. These studies indicate a common biochemical mechanism involved in the formation and release of SRS-A from these different tissues and cells and further confirm the observation that the rat
mast cell
is not a major source of SRS-A in the rat.
...
PMID:The effect of thiols on the immunologic release of slow reacting substance of anaphylaxis. II. Other in vitro and in vivo models. 5 39
X537A released histamine from isolated histamine-retaining
mast cell
granules incubated at 37 degrees C in Tris-
sodium
(150 mM) or Tris-potassium (150 mM), but not in Tris-glucose (300 mM). The release was depressed at 0 degrees C. In contrast, decylamine released all histamine bound to the granules irrespective of the presence of monovalent cations in the incubation medium of temperature. X537A did not release histamine from an artificial heparin-protamine complex when incubated in deionized water. The mechanism of histamine release by X537A can be explained by the ability of the ionophore to carry monovalent cations across cellular membranes, hereby making the ions available for exchange with histamine bound to the granular matrix. This mechanism can be distinguished from that of agents triggering an exchange between cations and bound histamine through a calcium- and energy-dependent exocytotic process on the one hand and through membrane lysis on the other. Based on the observation that the ionophore was able to carry histamine into the bulk of an organic phase, various possibilities exist to explain how histamine escapes from the cells following release from intracellular granular stores.
...
PMID:Mechanism of histamine release induced by the ionophore X537A from isolated rat mast cells. 7 63
Sodium glycocholate was shown to remove a Ca2+-activated adenosine triphosphatase from the external surface of the rat
mast cell
without causing lysis. Sensitized mast cells pretreated with
sodium
glycocholate showed a decrease in histamine-releasing capacity when triggered with antigen, Synacthen and ATP. Release induced by calcium ionophore A23187 was unaffected.
...
PMID:Effect of removal of calcium-activated adenosine triphosphatase from rat mast cells by treatment with sodium glycocholate. 7 27
The source of the histamine released during damage to the gastric mucosa has been investigated in rats using perfused total gastric pouches. Two groups of rats were treated with either intraperitoneal normal saline or compound 48/80, and agent that produces
mast cell
degranulation, over a 5-day period. On the 5th day, total gastric pouches were prepared and connected to a perfusion circuit that enabled a 20-ml volume to be circulated through the pouches. The experiments consisted of three 30-min periods during which transmucosal potential difference was monitored and ionic (hydrogen and
sodium
) flux measured; standard acid solution was used in the first two periods and a taurocholate solution in the third.
Sodium
taurocholate produced a significant increase in ionic flux and fall in the potential difference, the magnitude of the changes being similar in the 48/80- and saline-treated groups. Histamine was released from the mucosa in significantly greater amounts during the taurocholate period, and the increase was similar in both groups of rats. Histological examination of the stomachs confirmed
mast cell
degranulation in the 48/80-treated groups. We conclude that the histamine released during mucosal damage is probably derived from the "nonmast cell pool" and that this histamine may play a role in mediating the mucosal damage.
...
PMID:Effect of mast cell degranulation on gastric mucosal damage produced by sodium taurocholate in the rat. 7 16
We suggest a method for the section staining of polyanions by means of ruthenium red and osmium tetroxide. A 5 min incubation in diluted ruthenium red-OsO4 solution pH = 7.4 of ultrathin Durcupan-sections previously treated with
sodium
methoxide results in the opaque stining of
mast cell
granules, cartilage proteoglycans, and various epithelial mucosubstances.
...
PMID:[A ruthenium red-osmium tetroxide section staining method (author's transl)]. 9 Dec 93
Cromolyn is a prototype of a new series of drugs, the pharmacologic activities of which may offer an entirely new approach in the treatment of asthma. Whereas bronchodilator drugs and steroids act primarily at tissue sites to counteract the effects of various toxic mediators released from tissue mast cells, cromolyn prevents the release of such mediators from
mast cell
membranes. The advent of cromolyn
sodium
therapy has been recognized as a significant advance by the pharmaceutical industry, which is rapidly developing a series of cromolyn-like drugs with similar properties. Many of these compounds are active orally, and some preliminary investigations suggest that they also could be clinically effective. Cromolyn has therapeutic value in immunologic and nonimmunologically induced bronchospasm, being particularly suited for conditions amenable to long-term prophylactic therapy. The risk-to-benefit ratio of cromolyn
sodium
therapy is excellent. Cromolyn sodium is an important adjunct in the treatment of asthma. By topical administration the drug has been effective in seasonal and perennial rhinoconjunctivitis and in selected cases of gastrointestinal allergy to foods.
...
PMID:Therapy with cromolyn sodium. 9 84
The effect of inhalation of 2 per cent solution of
sodium
cromoglycate compared to that of saline on the bronchial response to methacholine and histamine was studied in 30 asthmatic children. Seven of 17 children challenged with methacholine showed decreased sensitivity after pretreatment with
sodium
cromoglycate. In 4 of 13 children,
sodium
cromoglycate attenuated the response to inhaled histamine. We conclude that in some asthmatic children,
sodium
cromoglycate provides significant protection against these nonallergenic challenges. This may have some therapeutic implications in the management of these patients. Our findings raise the possibility that
sodium
cromoglycate might have an action on cholinergic or irritant receptor sites in addition to inhibition of
mast cell
degranulation.
...
PMID:Sodium cromoglycate-induced changes in the dose-response curve of inhaled methacholine and histamine in asthmatic children. 11 Jan 85
Angiotensin-converting enzyme has been solubilized from a particulate fraction of rabbit lung and purified to apparent homogeneity in 11% yield by a procedure including fractionation with DEAE-cellulose and calcium phosphate gel, elution from Sephadex G-200, and lectin affinity chromatography. The molecular weight estimated by equilibrium sedimentation was approximately 129,000, either in the absence or presence of 6 M guanidine hydrochloride. A slightly higher value of 140,000 determined for the reduced, denatured protein by gel electrophoresis in the presence of
sodium
dodecyl sulfate and a much higher figure derived from gel filtration are probably due to the glycoprotein nature of the enzyme. Its oligosaccharide content accounted for 26% of the weight calculated from its amino acid and carbohydrate composition. The estimated content of sugar residues per mole was: galactose, 57; N-acetylglucosamine, 53; mannose, 43; N-acetylneuraminic acid, 19; and fucose, 4. Threonine and alanine were identified, respectively, as NH2-terminal and COOH-terminal residues by the dansylation procedure and by digestion with
carboxypeptidase A
. The enzyme was found to contain approximately 1 g atom of zinc per mol. Km values for hydrolysis of hippurylhistidylleucine and angiotensin I were 2.3 and 0.07 mM, and the corresponding turnover numbers were 15,430 and 792 mol/min/mol at 37 degrees. Bradykinin was also a substrate, and release of its COOH-terminal dipeptide, Phe-Arg, was catalyzed at a comparable rate to that of His-Leu from the COOH terminus of angiotensin I. Enzyme activity required the presence of chloride ions and was inhibited by EDTA and by low concentrations of Bothrops bradykinin-potentiating peptides. In addition, hydrolysis of hippurylhistidylleucine was inhibited competitively by other defined peptides, including di- and tripeptides, which were not substrates.
...
PMID:Pulmonary angiotensin-converting enzyme. Structural and catalytic properties. 16 57
High density lipoproteins were isolated from plasma of white Leghorn hens by ultracentrifugal flotation between densities 1.063 and 1.210 g/ml. After delipidation, the lipid-free proteins were fractionated by chromatography on Sephadex G-150 in urea; one major apolipoprotein was isolated and characterized. From its chemical, physical and immunochemical properties, the major apoprotein from hen high-density lipoproteins has characteristics similar to the major apoprotein of human high density lipoproteins, apoA-I. Thus the hen protein has been designated hen apoA-I. Hen apoA-I has a molecular weight of approximately 28 000 as determined by polyacrylamide gel electrophoresis in
sodium
dodecyl sulfate. Its calculated molecular weight from its 234 constituent amino acids is 26 674. Hen apoA-I differed from its human counterpart by containing isoleucine. Treatment of hen apoA-I with
carboxypeptidase A
yielded a COOH-terminal sequence of Leu-Val-Ala-Gln. Automatic Edman degradation of the apoprotein gave an NH2-terminal sequence of Asp-Glu-Pro-Gln-Pro-Glu-Leu. Hen apoA-I had a circular dichroic spectrum typical of alpha-helical structures; the calculated helicity was 90%. Goat antisera prepared to hen apoA-I formed precipitin lines of complete identity to the hen apoprotein but lines of only partial identity to human apoA-I. These studies show that the major apoprotein from hen and human high-density lipoproteins have similar properties to each other suggesting a common physiologic function.
...
PMID:Isolation and characterization of the major apolipoprotein from chicken high density lipoproteins. 17 37
Baboon high-density lipoproteins (HDL) were isolated by preparative ultracentrifugation between d = 1.063 and 1.215 g/mL. The HDL contains 48.8% protein and a lipid distribution similar to human HDL. The phospholipid distribution shows a low sphingomyelin value (5.9%), and the fatty acid composition of HDL is comparable to the human data except for the 18:1/18:2 ratio as a result of a higher 18:1 content in the CE and a lower 18:2 concentration in the PL. The major HDL apoproteins isolated on diethylaminoethyl-cellulose had a mobility on
sodium
dodecyl sulfate--polyacrylamide gel electrophoresis and a molecular weight and an amino acid composition similar to human apoA-I. However, the amino acid sequence of the first 30 residues of baboon apoA-I differed from the human apoprotein in residues 15 and 21. Treatment of apoA-I with
carboxypeptidase A
indicated a carboxyl-terminal sequence of Leu-Ser-Thr-Gln. Baboon apoHDL contained monomeric apoA-II with the mobility of monomeric human apoA-II and a molecular weight of 8500. The amino acid composition differed from the human apoA-II by the presence of arginine and by the absence of half-cystine and isoleucine. The circular dichroic spectra of apoA-I and apoA-II demonstrated a higher helicity compared to the human apoproteins. Recombination studies by microcalorimetry of apoHDL with dimyristoylphosphatidylcholine (DMPC) indicated similarities in the thermodynamic binding properties of the HDL apoproteins from man and baboon. The maximal-binding enthalpies of DMPC to apoHDL, apoA-I, and apoA-II were lower for the baboon than for the human apoprotein.
...
PMID:Characterization of baboon plasma high-density lipoproteins and of their major apoproteins. 19 55
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