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)

L-lactate dehydrogenase of the psychrophilic bacterium B. psychrosaccharolyticus was isolated by a three-step procedure and its total amino-acid sequence determined by automated Edman degradation. The protein consists of 318 amino-acid residues and its calculated molecular mass is 35,254 Da. Most of the primary structure could be established by sequencing large peptide fragments obtained by chemical cleavages, namely with BNPS-skatole and with CNBr. Further fragmentations of two tryptophan peptides with the endoproteinase Lys-C and with diluted HCl resulted in shorter overlapping peptides, the analysis of which completed the sequence. The C-terminal sequence Glu-Gln was established by carboxypeptidase A experiments and was then verified by the analysis of short C-terminal tryptic and chymotryptic peptides. The first lactate dehydrogenase sequenced so far of a psychrophilic bacillus shows sequence homologies between 60% and 75% to the enzymes from the mesophilic B. megaterium and B. subtilis and the thermophilic B. stearothermophilus, B. caldolyticus and B. caldotenax. Within the 50 N-terminal residues, three additional sequences could be included in our comparisons. In this part of the molecule, sequence homologies between 56% and 74% were calculated.
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PMID:The primary structure of the psychrophilic lactate dehydrogenase from Bacillus psychrosaccharolyticus. 343 42

Ethylcholine mustard aziridinium ion (AF64A, MEChMAz) has been proposed as a cholinergic neuron-specific neurotoxin. We report that in further studies on its mechanism of action incubation of the cholinergic neuroblastoma X glioma cell line, NG-108-15, with 100 microM AF64A resulted in a rapid decrease in cellular choline acetyltransferase (ChAT) activity which preceded cytotoxicity. Thus, a 60-85% decrease in ChAT activity was measured within 5 h of AF64A exposure, whereas cell lysis (measured as the release of the cytosolic enzyme lactate dehydrogenase into the medium) did not become apparent until 18 h of AF64A exposure. This led us to examine the effects of AF64A on partially purified ChAT. We report a concentration- and time-dependent inhibition of partially purified ChAT by AF64A that could not be reversed by dialysis but could be prevented by coincubation of the enzyme and AF64A with choline but not with acetyl-coenzyme A. We present kinetic evidence that choline and AF64A compete for the same site on the enzyme. In addition, thiosulfate, which inactivates the aziridinium ion, eliminated AF64A's capacity to inhibit the enzyme. AF64A also irreversibly inhibited partially purified choline kinase and acetylcholinesterase but not lactate dehydrogenase, alcohol dehydrogenase, carboxypeptidase A, or chymotrypsinogen, enzymes that do not use choline as a substrate or product. Thus, the data suggest that AF64A acts as an irreversible active site directed inhibitor of ChAT and possibly other enzymes recognizing choline.
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PMID:AF64A: an active site directed irreversible inhibitor of choline acetyltransferase. 383 98

Protamine sulfate, known for a long time as a histamine releaser, was labeled with a fluorescent dye (FITC). This conjugate was shown to stain selectively the mast cell fraction of rat peritoneal cells. Within a few seconds, the protamine was found inside the cells. Although the cells had lost their histamine completely, no granules were found outside the cells. In the electron microscope, the protamine treated mast cells showed a loss of the electron density of their granules, a vacuolization, and other signs of histamine release. Evidence for a direct connection between the vacuoles and the extracellular fluid was gained by incubating mast cells in FITC-labeled human serum albumin followed by the addition of unlabeled protamine. After washing, the fluorescence was found to be located inside the cells, demonstrating an influx of the FITC-HSA under the influence of protamine. The protamine-induced release reaction is increased after addition of Ca2+, reduced by lowering the temperature, addition of 2-deoxyglucose, or cytochalasin B. Disodium cromoglycate also diminished the histamine release in a dose dependent manner. Protamine did not induce a loss of lactate dehydrogenase from the mast cells. The release reaction is mediated by the cell membrane, as shown by the releasing activity of insolubilized protamine. We conclude that the protamine-induced release is a non-cytotoxic reaction, fulfilling some criteria of the anaphylactic histamine release.
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PMID:[Mode of action of protamine sulfate on histamine secretion in the rat mast cells]. 616 92

The specific activities of pyruvate kinase and phosphofructokinase but not lactate dehydrogenase increase as P-815 mastocytoma cells approach the stationary phase. During this growth period, the rates of uptake of labelled precursors into DNA, RNA and total protein decreases. On the other hand, the pyruvate kinase protein level changes in parallel with activity. Although the K-isozyme is the primary form of pyruvate kinase expressed, some M-type subunit is also present and both forms undergo an increase in specific activity. In addition, pyruvate kinase expression is also elevated by adding cAMP analogues with theophylline, butyrate or conditioned media. This increased level of expression is hypothesized to be a secondary event associated with a differentiation-like-induced expression of the mast cell phenotype.
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PMID:Regulation of pyruvate kinase expression and growth in mastocytoma cells. I. Initial observations. 619 20

Based on the partial sequence of the cyanogen bromide fragments [Tratschin, J.D., Wirz, B., Frank, G. and Zuber, H. (1983) Hoppe-Seyler's Z. Physiol. Chem. 364, 879-892], the amino-acid sequence of thermophilic lactate dehydrogenase from B. stearothermophilus was completed by the preparation and sequencing (sequenator, carboxypeptidase A and Y) of further overlapping fragments. Suitable peptide fragments were obtained by lactate dehydrogenase cleavage with hydroxylamine, o-iodosobenzoic acid and trypsin. The polypeptide chain of thermophilic lactate dehydrogenase from B. stearothermophilus consists of 317 amino-acid residues. While sequence homology with mesophilic lactate dehydrogenase of higher organisms reaches 35%, it is substantially higher with this mesophilic enzyme of bacillae (greater than 60%, B. megaterium, B. subtilis). The secondary structure elements and amino-acid residues of the active site of thermophilic lactate dehydrogenase deducted from primary structure data were compared with those from the mesophilic enzyme, the same was done for the internal sequence homology at the nucleotide-binding units. A comparative structure analysis (matrix system) based on the primary structure data of thermophilic enzyme should provide insight into the characteristic structure differences between thermophilic and mesophilic lactate dehydrogenase.
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PMID:Structure and function of L-lactate dehydrogenases from thermophilic and mesophilic bacteria. III) The primary structure of thermophilic lactate dehydrogenase from Bacillus stearothermophilus. Hydroxylamine-, o-iodosobenzoic acid- and tryptic-fragments. The complete amino-acid sequence. 635 52

Highly purified porcine phospholipase A2 induced noncytotoxic rat cell degranulation, as indicated by release of histamine without release of the cytoplasmic marker lactate dehydrogenase. Ultrastructural studies using transmission, scanning, and freeze fracture electron microscopic techniques indicated that phospholipase A2-induced degranulation was comparable to that caused by other mast cell secretagogues. Secretory changes noted were fusion of perigranular and plasma membranes, formation of vacuoles containing less electron-dense granules, and exocytosis of the altered granules through pores in the plasma membrane, without alteration in other intracellular organelles. The earliest consistent feature of the exocytotic process (within 1 minute) was the formation of plasma membrane bulges overlying cytoplasmic granules, with depletion of intramembranous particles from the bulges and a reduction in surface microridges. Phospholipase A2-induced mast cell degranulation was blocked by the phospholipase inhibitor 4-bromophenacyl bromide and by eicosa-5,8,11,14-tetraynoic acid (ETYA) but not by indomethacin. Since ETYA inhibits both the cyclooxygenase and lipoxygenase pathways of arachidonic acid metabolism and indomethacin only the cyclooxygenase pathway, these findings are compatible with the mediation of phospholipase A2-induced mast cell degranulation by a lipoxygenase product of the released arachidonic acid ETYA, however, may inhibit phospholipase activity directly and thus affect degranulation by phospholipase A2 in this way. These studies indicate that phospholipase A2 can induce mast cell degranulation and provides evidence that is compatible with, but not proof of, mediation of this process by a lipoxygenase product of arachidonic acid metabolism.
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PMID:Phospholipase A2-induced rat mast cell secretion. Role of arachidonic acid metabolites. 681 79

Cultured rat embryonic skin fibroblasts phagocytosed rat mast cell granules added to the medium or released from co-cultured mast cells by rabbit anti-rat IgE or Compound 48/80. Electron microscopy of fibroblasts incubated with mast cell granules revealed that granules adjacent to the plasmalemma were engulfed by long, thin cytoplasmic processes. Internalization proceeded to fusion of encircling processes and formation of phagosomes. Microtubules and 60 A microfilaments became closely associated with the phagosomal membrane to which small vesicles and cisternae of endoplasmic reticulum fused. The rate of uptake of mast cell granules by fibroblasts was dependent upon temperature and granule concentration. Cytochalasin B inhibited granule uptake whereas colchicine and nocodazole had little effect. Phagocytosis was not influenced by actinomycin D and cycloheximide, was partially inhibited by fluoride, and was markedly inhibited by cyanide, azide, and 2,4-dinitrophenol. Supernatants from fibroblast cultures incubated with mast cell granules for 24 and 48 hr, during which period phagocytosis occurred, contained elevated levels of collagenase and beta-hexosaminidase, but normal levels of lactate dehydrogenase and superoxide dismutase. These results support the concept that immediate hypersensitivity reactions are in part terminated by phagocytosis of biologically active discharged mast cell granules by resident connective tissue fibroblasts. Further, it is suggested that a consequence of this process is an alteration in fibroblast behavior, providing a unique link between immediate hypersensitivity reactions and connective tissue responses to inflammation.
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PMID:Phagocytosis of mast cell granules by cultured fibroblasts. 684 86

The authors describe the results of a series of cytochemical, autoradiographic, cytophotometric and immunological investigations carried out in a case of tissue mast cell leukaemia. Leukaemic mast cells showed certain distinctive cytochemical features, amongst which an intense periodic acid-Schiff (PAS) reaction, sensitive to amylase digestion, strong naphthol AS-D chloroacetate esterase (NASDCE), intense lactate dehydrogenase (LD) activity. Proliferative activity, determined autoradiographically with 3H-dT, was considerably low and was mainly confined to the larger cells. Also uridine and leucine incorporation were markedly reduced. Microdensitometry disclosed that the mast cell population was mainly arrested in the G1 phase. Because of previous attempts to destroy selectively neoplastic tissue mast cells with sheep antihuman IgE serum, a search for surface bound IgE was carried out, but gave a negative result. Possible therapeutic approaches are considered in the light of previous clinical experience and on the basis of the results of the kinetic and metabolic studies.
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PMID:Cytobiological and clinical aspects of tissue mast cell leukaemia. 737 28

Precooling of the tissues was investigated as a possible means of reducing the thermal damage during CO2 laser surgery of the oral mucosa. Standard wounds 5 mm long were created with the CO2 laser, with and without precooling, or the scalpel on the dorsum of tongues. Tissue damage was evaluated by studying changes in mast cells and in the activity of lactate (LDH) and succinate (SDH) dehydrogenase. Cooled unoperated tongues acted as controls. The area of thermal damage, indicated by loss of SDH activity, was significantly smaller in precooled tissues (p < 0.001). Although a similar pattern was detected using LDH, the difference was not significant. At both 0 and 6 h normal mast cell numbers were significantly different between groups (p < 0.02). Furthermore, at 0 time, there were significant differences in the numbers of degranulated mast cells between surgical treatment groups (p = 0.001), although not at 6 h. Total numbers of mast cells (normal and degranulated) did not differ between treatment groups or between 0 and 6 h sampling times. Positive significant correlations were observed between the cross-sectional areas and widths of non-reactive succinate and lactate dehydrogenase and the number of degranulated mast cells around the laser wounds. Analysis of the data demonstrated that (i) uncooled laser wounds but not precooled laser wounds were associated significantly with greater levels of immediate mast cell degranulation than scalpel wounds (p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of thermal damage in precooled CO2 laser wounds using biological markers. 839 41

In the present study, we evaluated the potential role of mast cell degranulation in acute hypoxia/reoxygenation-induced injury to cardiomyocytes in the isolated rat heart. Histamine release was determined to delineate the extent of mast cell degranulation, whereas the release of creatine kinase (CK) and lactate dehydrogenase (LDH) was assessed to quantitate the extent of irreversible injury to cardiomyocytes. The suitability of peroxidase (PO) as a marker for mast cell degranulation was also evaluated. Reoxygenation resulted in a release of histamine corresponding with 6.5% +/- 0.6% of total tissue content, whereas LDH, CK and PO release amounted to 30% +/- 2%, 28% +/- 2% and 32% +/- 3% of their respective tissue contents. Identical perfusion in the presence of the mast cell stabilizer lodoxamide tromethamine resulted in a reduced histamine release (2.8% +/- 0.1%) of total tissue content upon reoxygenation, but the release of LDH, CK or PO was not influenced. Cumulative histamine release did not correlate with the amount of LDH, CK or PO released. Treatment with consecutive bolus injections of the mast cell degranulating compound 48/80 during normoxic perfusion resulted in an almost complete histamine release, whereas PO release remained below detection limit. When the compound 48/80-treated hearts were subjected to hypoxia/reoxygenation, the release of LDH, CK or PO during reoxygenation again remained unchanged, whereas histamine release was negligible. Determination of PO activity of freshly isolated cardiomyocytes demonstrated that the bulk of PO in rat hearts was located in this particular cell type. Therefore we conclude that in the isolated rat heart, PO release is not a specific marker of mast cell degranulation. In addition, our data provide no firm evidence that in this experimental model, mast cell degranulation contributes to a significant extent to acute hypoxia/reoxygenation-induced injury to cardiomyocytes.
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PMID:Lack of evidence for a role of mast cell degranulation in acute hypoxia/reoxygenation-induced injury in the isolated rat heart. 872 68


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