Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histamine release from isolated mast cells stimulated with somatostatin resembled that induced by other basic agents. The process was rapid, independent of added calcium or phospholipids, non-cytotoxic, species and tissue specific, not mediated through cell-fixed antibodies or glucoreceptors, and inhibited by antagonists of the polyamine receptor. Somatostatin and other polycations may then act through a common receptor or binding site on the mast cell membrane.
 ...
PMID:Histamine secretion from mast cells stimulated with somatostatin. 245 92

It has been shown that plasma histamine significantly increases during myocardial infarction in the dog. Histamine is also released when the isolated guinea-pig heart is reperfused after 30 minutes of low flow perfusion. The release of histamine and lactate dehydrogenase (LDH) after left anterior descending coronary artery ligation and release were investigated in the present study and related to the changes in electrocardiographic parameters and to a computer-aided analysis of left ventricular mast cell metachromasia. Spontaneous release of histamine was unchanged during ischemia and increased after the release of the ligature, while we observed a steady increase of LDH overflow. In parallel, a significant diminution of mast cell granule metachromasia was observed in left ventricular samples. The perfusion of the heart with FeCl3/ADP (10 microM/100 microM), a free radical-generating system, significantly enhanced both the basal and ischemic-reperfusion release of histamine, while perfusion with N-t-butyl-phenyl-nitrone (BPN/100 microM) a "spin-trapper" molecule, significantly decreased histamine and LDH release and the loss in metachromasia of left ventricular mast cells induced by reperfusion. Inhibitors of xanthine oxidase (allopurinol, 10 microM) and of calcium-activated proteases (leupeptin, 10 microM) modified the kinetics of histamine and LDH release.
 ...
PMID:Histamine release in acute coronary occlusion-reperfusion in isolated guinea-pig heart. 245 99

The release of histamine from rat mast cells induced by anti-immunoglobulin E (IgE) was markedly inhibited by Bowman-Birk soybean protease inhibitor (BBI) and anti-chymase F(ab')2 fragments which inhibit chymase activity [Kido, H., et al. (1985) Biochem. Int. 10, 863-871, and Fukusen, et al. (1987) Biochem. Med. Metab. Biol. 38, 165-169]. When radioiodinated anti-chymase F(ab')2 fragments or BBI were incubated with mast cells at 37 degrees C, they were subsequently recovered in the fractions of mast cell granules and of plasma membranes by Percoll density gradient centrifugation. However, when they were incubated with mast cells at 0 degrees C, they had no effect on histamine release and were subsequently recovered only in the plasma membrane fraction. Histamine release from mast cells was suppressed dose-dependently by the antibodies or BBI accumulated in mast cell granules at 37 degrees C. These results suggest that the antibodies and BBI are incorporated into mast cell granules and inhibit chymase activity, resulting in inhibition of histamine release.
 ...
PMID:Antibodies and inhibitor of chymase are incorporated into mast cell granules and inhibit histamine release. 246 36

A variety of basic, sensory neuropeptides induced the release of histamine from rat peritoneal mast cells. However, a wide range of other polycationic agents, such as compound 48/80, the mast-cell-degranulating peptide from bee venom and polylysine also activated this cell type. Histamine release induced by all of these agents had characteristic features in common. In each case, the process was extremely rapid, essentially independent of added calcium or phospholipids, not mediated through cell-fixed antibodies, and inhibited by antagonists of the so-called polyamine receptor. The release was also very species- and tissue-specific. All of the compounds were most active against rat serosal mast cells. Tissue mast cells of this species and peritoneal mast cells of other rodents showed graded responses while guinea pig and human mast cells were unreactive. On the basis of these results, the possible role of peptide-mast cell interactions in neurogenic models of inflammation is discussed.
 ...
PMID:Characteristics of histamine secretion induced by neuropeptides: implications for the relevance of peptide-mast cell interactions in allergy and inflammation. 246 10

Tryptase, a neutral protease of human mast cells, is a potentially important indicator of mast cell involvement in various clinical conditions. The current study examined the time course of appearance and disappearance of tryptase in the circulation after an anaphylactic event and the stability of both endogenous and exogenous tryptase in terms of freeze-thawing and temperature. The peak level of tryptase after an experimentally induced systemic anaphylactic reaction occurred 1-2 h after the initiating bee sting in each of three subjects, in contrast to histamine levels which peaked at 5-10 min. In some cases elevated levels of tryptase may not be detected during the initial 15-30 min. Tryptase levels then declined under apparent first order kinetics with a t1/2 of approximately 2h. Similar disappearance kinetics were observed for two subjects presenting in the emergency room with immediate type reactions, one with severe asthma after indomethacin ingestion, the other with systemic anaphylaxis after a bee sting. Histamine levels declined rapidly and were back to baseline by 15-60 min. Measured levels of tryptase in serum or plasma were not diminished by up to four freeze-thaw cycles. Incubation of serum samples taken from subjects with elevated levels of tryptase at 22 and 37 degrees C indicated that greater than 50% of endogenous tryptase was still detected after 4 d. Purified tryptase added to serum or plasma and incubated as above was less stable: approximately 50% of exogenous tryptase in serum and approximately 15% in plasma was detected after 2d of incubation. Therefore, optimally samples should be stored frozen, but even those stored at room temperature for up to 4 d should be satisfactory. The best time to obtain samples for tryptase determinations is 1-2 h after the precipitating event, but depending on the magnitude of the initial response elevated levels of tryptase may be present in the circulation for several hours.
 ...
PMID:Time course of appearance and disappearance of human mast cell tryptase in the circulation after anaphylaxis. 246 89

Rat mast cells were challenged with compound 48/80 or calcium ionophore A23187, and protein kinase C activity in the cell pellets and the amount of histamine release into the supernatant were measured. After stopping the reaction, rat mast cells were lysed in a medium which prevents alterations in phosphorylation and dephosphorylation during sample processing. Histamine was significantly released from compound 48/80-stimulated mast cells at 30 s after the stimulation. In parallel with this, protein kinase C activity in the cell pellets increased at 30 s and 1 min and returned to basal value 3 min after the stimulation. When mast cells were incubated with various concentrations of 48/80 for 30 s, the amount of histamine release and protein kinase C activity increased dependently on the concentration of 48/80. Significant histamine release from A23187-stimulated mast cells was found at 1 min after the stimulation. Also protein kinase C activity in the cell pellets increased at 1 min and returned to basal value 5 min after the stimulation. A reduction of cytosolic protein kinase C activity was observed upon 48/80 treatment in a time- and concentration-dependent manner. Further, staurosporine, a potent inhibitor of protein kinase C, inhibited 48/80-induced histamine release in parallel with the inhibition of protein kinase C activity. These findings suggest that transient increase of protein kinase C activity may be involved in the mast cell activation process.
 ...
PMID:Changes in protein kinase C activity during histamine release from activated rat mast cells. 246 47

Although mast cells and interferons are both involved in numerous immune and inflammatory responses, little is known about how microenvironmental factors such as interferons (IFNs) influence mast cell function. To study this question, sensitized peritoneal mast cells (greater than 98% purity) obtained from rats infected 4 weeks earlier with the parasite Nippostrongylus brasiliensis were preincubated for 24 hr with rat IFN-alpha/beta in RPMI-1640, then stimulated to degranulate with worm antigens. In the absence of antigen, IFN-alpha/beta had no noticeable effect on histamine release. However, in the presence of antigen, IFN-alpha/beta (150-1500 U/ml) inhibited histamine release in a dose-dependent manner (22.2 +/- 7.5% to 56.3 +/- 6.9%, n = 10). This inhibitory effect was neither heat (56 degrees for 1 hr) nor acid (pH 2 for 18 hr) labile, but was completely blocked by anti-IFN antibodies. In the presence of compound 48/80 (1 microgram/ml) or substance P (5 X 10(-5) M), IFN-alpha/beta was ineffective at modulating histamine release. Histamine release induced by antigen in the presence of the membrane phospholipid phosphatidyl-serine (30 micrograms/ml) was inhibited by IFN in a dose-dependent manner, but maximal inhibition (25.3 +/- 2.7%, n = 10) was reached at a lower concentration of IFN (750 U/ml) than when antigen was used alone. Therefore, rat IFN-alpha/beta appears to inhibit histamine release from rat mast cells in a dose- and stimulus-dependent manner and may do so by reducing the fluidity of the cell membrane.
 ...
PMID:Interferon-alpha/beta inhibits IgE-dependent histamine release from rat mast cells. 246 45

Histamine was released from mast cells in isolated perfused heart and kidney of the rat, but not from mast cells in guinea-pig tissues, by a substance P (SP) analogue (SP(1-4)-NH-C12H25), SP(1-4)-C12 for abbreviation. This peptide also released histamine from peritoneal mast cells and basophil leucocytes of the rat. Substance P itself was compared with SP(1-4)-C12 and some structurally related peptides and showed weaker activity. SP(1-4)-C12 also released leukotrienes C4, D4, E4 and thromboxane B2 from rat heart. However, there was little effect on heart rate and force of contraction and no effect on perfusion pressure (vascular resistance) of either rat heart or kidney. The findings demonstrate the structural requirements for histamine release by SP (a possible mediator of 'neurogenic' inflammation), the metabolic energy-dependence of the release process and the functional heterogeneity and interspecies differences in mast cell populations.
 ...
PMID:Substance P and Arg-Pro-Lys-Pro-NH-C12-H25-induced mediator release from different mast cell subtypes of rat and guinea-pig. 247 Jun 97

Populations of mature, long-lived, nondividing mast cells develop on embryonic fibroblast monolayers after 1 mo growth of lymph node cells taken from mice immunized with horse serum. Total mast cell degranulation with 80-90% histamine release has been obtained by monoclonal anti-2,4-dinitrophenol (anti-DNP) IgE and the antigen. This degranulation process was studied by time-lapse cinematography and scanning electron microscopy. Excitation of the mast cells began as early as 10 s after addition of the antigen and lasted for about 15 s. Consequently, the fibroblast cytoplasm was displaced by short 5-10 s movements. Before degranulation, due to an extracellular film that coated the cells and the extracellular fibers, the monolayer appeared as a continuous, uninterrupted layer. After degranulation and fibroblast cytoplasm displacement, the fibrous network was exposed. Several inhibitors and antagonists of mast cell mediators were introduced to the cultures prior to addition of the antigen. So far, only with soybean trypsin inhibitor was the cytoplasm dislocation inhibited. Histamine H1 and H2 and serotonin receptor antagonists, as well as indomethacin, cortisol, aprotinin, and phenylmethylsulfonyl fluoride, did not inhibit. These results suggest that chymase, which constitutes the greater part of the mast cell granule protein, is the causative agent.
 ...
PMID:Structural alterations in fibroblast monolayers caused by mast cell degranulation. 247 Aug 46

1. Medium conditioned by rat neutrophils stimulated by N-formyl-methionyl-leucyl-phenylalanine (FMLP) has been found to generate mast cell histamine-releasing activity (HRA) when incubated with bovine serum albumin (BSA). 2. Histamine release increased as the concentration of BSA used to generate HRA was increased from 0.25 to 10 mg ml-1, as the concentration of neurotrophil conditioned medium was increased and as the concentration of FMLP used to stimulate the neutrophils was increased. Histamine release was non-cytotoxic as it was inhibited by energy deprivation or by removal of calcium and it was accompanied by degranulation. 3. HRA was detectable after 30 min of incubation with BSA and its generation continued to increase over the 18 h of our measurements. 4. Generation of HRA was dependent upon the presence of medium from stimulated neutrophils and on the presence of BSA, although plasma could substitute for BSA. Likewise, HRA could be generated from gamma-globulin although to a lesser extent than with albumin. 5. Generation was optimum at acid pH and was inhibited by prior boiling of the neutrophil conditioned medium or by the addition of pepstatin. 6. It is suggested that an enzyme(s) released from the neutrophil during stimulation acts on an albumin-like substrate to generate HRA. It is proposed that HRA is peptide in nature and may be generated during an inflammatory response.
 ...
PMID:Generation of histamine-releasing activity from serum albumin by medium derived from stimulated neutrophils of rat. 247 47


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>