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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have investigated the possible role of guanine nucleotide-binding proteins in the process of antigen-induced exocytosis in a cultured rat mast cell line, RBL-2H3 cells. The mRNAs for the alpha subunits of the guanine nucleotide-binding proteins G alpha S (short and long forms), G alpha i-2, G alpha i-3, and G alpha Z were detected by hybridization with G alpha-specific oligonucleotide probes. The corresponding proteins were identified in membranes of RBL-2H3 cells on the basis of size, immunoreactivity with specific antibodies, and their ability to serve as substrates for ADP-ribosylation by cholera toxin or pertussis toxin. Treatment of cells with as little as 10(-9) to 10(-7) M dexamethasone markedly decreased the amount of G alpha Z mRNA and membrane G alpha Z, as well as the responsiveness of the cells to antigen stimulation. In the same cells, the exposure to dexamethasone caused an increase in the amounts of certain other G alpha subunits, particularly G alpha i-3, and in the responsiveness of the cells to an adenosine analog, N(ethylcarboxamido)-adenosine. Because of the apparent decrease in G alpha Z mRNA and protein in dexamethasone-treated cells and the fact that neither cholera toxin nor pertussis toxin inhibits the stimulatory signals to antigen [J. Biol. Chem. 265:745-753 (1990)], we suggest that G alpha Z is a potential candidate for regulating the early signals in antigen-stimulated RBL-2H3 cells.
Mol Pharmacol 1991 Oct
PMID:GTP-binding protein G alpha Z: its down-regulation by dexamethasone and its credentials as a mediator of antigen-induced responses in RBL-2H3 cells. 192 83

Recent studies have led to a rapid expansion of knowledge concerning the structure and biology of the two major mast cell proteinases, tryptase and chymase. Tryptase is an abundant, trypsin-like enzyme found in the secretory granules of all human lung mast cells. The subunits of the heparin-associated tryptase tetramer appear to be the products of a multigene family whose intron-exon organization is unique and is not closely related to that of other mast cell or leukocyte serine proteinases. In vitro studies suggest that tryptases may participate in lung and airway responses by regulating airway neuropeptide activity, bronchomotor tone, and fibroblast mitogenesis. Mast cell chymases are chymotrypsin-like proteinases related closely to neutrophil cathepsin G and lymphocyte granzymes. The cDNA-derived structures of tryptase and chymase suggest that the two enzymes may differ in modes of activation from proenzyme forms, although the mature enzymes are packaged and released together. Chymase expression appears to be limited to a subset of human lung mast cells most prevalent in the airway submucosa. Possible roles for chymase include inactivation of sensory neuropeptides, regulation of submucosal gland secretion, and potentiation of histamine-induced vascular permeability.
Am J Respir Cell Mol Biol 1991 May
PMID:The structure and airway biology of mast cell proteinases. 202 78

We have previously characterized dog mastocytoma cells propagated in nude mice. We have established two of these lines (C1 and C2) in continuous culture. Freshly disaggregated mastocytoma cells were cultured in Dulbecco's modified Eagle's medium (DME)-H16 mixed with 50% Ham's F12 and supplemented with histidine and 5% allergic dog serum (ADS). Cells were fed every 3 d and passaged weekly. Growth was assessed by cell count. Cell growth was best supported by culture in 5% ADS. C1 cells grow in suspension in ADS and have been passaged 55 times with a doubling time of 37.4 +/- 18.7 h (mean +/- 1 SD; n = 15). C2 cells adhere to tissue culture plastic in ADS and have been passaged 26 times with a doubling time of 49.3 +/- 12.5 h (n = 13). Morphologic and functional characteristics are unchanged from those described in cells propagated in nude mice. Histamine content for C1 is 0.46 +/- 0.18 pg/cell (n = 12) and 0.07 +/- 0.04 pg/cell (n = 6) for C2. Both lines contain the neutral protease tryptase and C2 contains chymase. Calcium ionophore A23187 or ragweed antigen caused concentration-dependent histamine release from both cell lines. C1 and C2 generate prostaglandin D2 in response to A23187. We conclude that dog mastocytoma cells can be established in continuous culture, thus providing a system for studying mast cell biology, including growth and development.
Am J Respir Cell Mol Biol 1990 Nov
PMID:Establishment of two dog mastocytoma cell lines in continuous culture. 212 Nov 70

Irradiation with a single dose of 30 Grey on the basal regions of the lungs of Sprague-Dawley rats induced a peribronchial and alveolar inflammation. Infiltration of mast cells in the edematous alveolar interstitial tissue and also in the peribronchial tissue were characteristic features of the lesion. The appearance of mast cells was already seen 4 wk after irradiation and by weeks 6 to 8 there was a heavy infiltration. The staining properties suggested that they were connective tissue-type mast cells. The infiltration of mast cells was paralleled by an accumulation of hyaluronan (hyaluronic acid) in the alveolar interstitial tissue 6 and 8 wk after irradiation. The recovery of hyaluronan (HA) during bronchoalveolar lavage (BAL) of the lungs also increased at this time. Treatment with a mast cell secretagogue, compound 48/80, induced a distinct reduction of granulated mast cells in the alveolar tissue. Regular treatment with compound 48/80 from the time of irradiation considerably reduced the HA recovery during BAL and the HA accumulation in the interstitial tissue but did not affect the interstitial infiltration of mononuclear cells and polymorphonuclear leukocytes. By contrast, an accumulation of HA in the alveolar interstitial space was induced when compound 48/80 was given not until mast cell infiltration of the lung had started. The effects of compound 48/80 indicate that the connective tissue response after lung irradiation is dependent on whether or not mast cell degranulation is induced before or after the mast cell infiltration of the alveolar tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Respir Cell Mol Biol 1990 Feb
PMID:A mast cell secretagogue, compound 48/80, prevents the accumulation of hyaluronan in lung tissue injured by ionizing irradiation. 230 75

Myofiber injury-repair was studied in the rat following blunt trauma to the lower leg in order to understand how the inflammatory and regenerative responses of muscles are altered when myofiber rupture is accompanied by bleeding and clotting reactions. A contusion injury to the muscles of the lower hindlimb of the rat was induced by applying an impact force of 4.7 N-m/cm2 to one leg. The gastrocnemius and soleus muscles were removed bilaterally and evaluated by histochemical and immunohistochemical techniques to document myofiber, vascular, and connective tissue alterations for several days following insult (6-120 hr). A significant increase in wet weight of the gastrocnemius muscle was noted 24 hr postinjury as fluid accumulation and bruising were evident in the muscles resulting from bleeding and inflammation. Vascular disruption was confirmed by the localization of some plasma constituents (fibrinogen, albumin, and complement C3) throughout the interstitial space and even inside some of the damaged myofibers. Inflammation was present and persisted for 5 days as evidenced by continued mast cell degranulation and increased vascular permeability. Using antibodies to identify specific proteoglycans which appear or disappear at various times during muscle regeneration, muscle repair could be followed. The repair process required approximately 10 days for restoration of morphologically intact myofibers. Thus, myofiber repair processes appear to be maintained even after disruption of the vascular system and ischemia following blunt trauma.
Exp Mol Pathol 1990 Feb
PMID:Extracellular matrix changes following blunt trauma to rat skeletal muscles. 230 15

The histamine content of uteri from mice was analyzed in terms of both concentration and total amount per uterine horn a) at two stages of the estrous cycle (estrous and diestrous), b) under sex hormone treatment, c) during pregnancy and after delivery. Histamine concentration and mast cell density were greater during diestrous and in mice treated with progesterone (p less than 0.001). This effect was attributed to a reduction in uterine mass weight, since the amount of histamine per uterine horn remained constant throughout the estrous cycle. During pregnancy, both concentration and amount of histamine per uterine horn were increased, values were significantly higher than in estrous (p less than 0.001) from day 14-17 until day 21 when labor occurred. After six to eight hours post-partum an abrupt reduction on histamine content was observed. Mast cells were more abundant in myometrium than in endometrium, their density followed the same pattern as histamine concentration throughout the estrous cycle.
Cell Mol Biol 1990
PMID:Histamine content and mast cells distribution in mouse uterus: the effect of sexual hormones, gestation and labor. 233 18

Structural heterogeneity of mast cells in human bronchial mucosa was investigated by examining 100 cells by electron microscopy and morphometry. Differential counts of secretory granules allowed subdivision of mast cells into three groups: (1) 49 cells with greater than 65% mixed granules; (2) 30 cells with greater than 30% scrolled granules; (3) 12 cells with greater than 30% particulate granules. Nine cells showed borderline characteristics. Records of depths of cells in the mucosa showed that most mixed-granule cells occupied middle levels, whereas most scrolled granule cells lay higher up, near the basement membrane. This raised the possibility that scrolled-granule cells may represent partly degranulated mixed-granule cells. Nineteen mast cells were filled with very dense mixed granules, and appeared to correspond to those staining with safranin in paraffin sections. However, morphometry did not produce any criteria for distinguishing these cells sharply from paler mixed-granule cells, which were therefore regarded as degranulating forms of the same type of cell. Evidence was found of a gradient of mast cell degranulation which appeared to increase in magnitude upward from deep submucosa to superficial mucosa. This evidence included finding a significant upward reduction in total granule area per cell, total granule numbers, numbers of mixed granules, and numbers of dense-cored granules. It was concluded that although bronchial mucosal mast cells could be subdivided ultrastructurally into three apparently heterogeneous groups, degranulation was found to produce a wide range of different cell appearances, and could, conceivably, even be responsible for the above grouping, rather than intrinsic mast cell heterogeneity.
Am J Respir Cell Mol Biol 1990 Jul
PMID:Heterogeneous ultrastructure of human bronchial mast cells: morphometric subdivision of cell types and evidence for a degranulation gradient. 236 37

Polyclonal antisera with pre-determined specificities for a range of rat IgE epitopes were produced by immunizing rabbits with KLH-conjugates of five different synthetic peptides representing sequences 378-396, 414-428, 491-503, 522-535 and 560-571 in the CH3 and CH4 domains of rat IgE. Each rabbit elicited peptide-specific antibodies which were capable of binding affinity-purified rat IgE (IR162) (titres 1/1000-1/10,000) and IgE in rat immunocytoma serum (IR162) either immobilized on microtitre-plates or in free-solution as assessed by ELISA. Heating a solution of rat IgE at 56 degrees C for 1 hr, a treatment known to abolish the cytophilic activity of rat IgE and also induce irreversible conformational changes in the CH3 and CH4 domains, resulted in enhanced binding of the immunoglobulin to antibodies directed against IgE sequences represented by two of the synthetic peptides 414-428 and 491-503, but not to the three other peptides. The five anti-peptide sera together with two previously studied antisera specific for rat IgE sequences 459-472 and 542-557 were tested in functional assays designed to investigate the mode of interaction between rat IgE and its receptor on rat mast cells. Each anti-peptide serum was capable of inhibiting the binding of IgE to mast cells and furthermore, able to initiate the secretion of histamine from cells sensitized with rat IgE in an "anti-IgE"-induced manner. In view of the evidence implicating the CH3 and/or CH4 domains as the location of the mast cell receptor-site on rat IgE, we propose a model to describe the mode of interaction between IgE and its mast cell receptor.
Mol Immunol 1987 Apr
PMID:Analysis of the interaction between rat immunoglobulin E and rat mast cells using anti-peptide antibodies. 244 34

Degranulation of IgE-sensitized rat mast cells by antigen was studied quantitatively in vitro and in vivo by electron microscopy. The inhibition of this degranulation by an anti-allergic drug, N-(3,4-dimethoxycinnamoyl)anthranilic acid (Tranilast), was also examined both in vitro and in vivo. In the in vitro study using peritoneal mast cells, alteration of the granules, cavity formation by fusion of the perigranular membrane and granule discharge due to fusion of the cavity membrane with the cell membrane were observed and were accompanied by histamine release. Scanning electron microscopy disclosed the extrusion of smooth, round bodies from pores formed on the cell surface. In the in vivo study of passive cutaneous anaphylaxis (PCA), the characteristic features of mast cell degranulation were obvious 5 min after the injection of antigen; leakage of dye increased progressively from 5 to 30 min but was not found at 6 h. From quantitative analysis of the substructure of mast cells, it was demonstrated that degranulation of IgE-sensitized mast cell induced by antigen was achieved by sequential exocytosis both in vitro and in vivo. Tranilast inhibited these changes to a remarkable extent and it was concluded that the inhibition of mast cell degranulation by this drug might play an important role in anti-allergic treatment.
Virchows Arch B Cell Pathol Incl Mol Pathol 1988
PMID:Mast cell degranulation and its inhibition by an anti-allergic agent tranilast. An electron microscopic study. 245 82

Autocrine interleukin 3 (IL-3)-secreting tumors were generated from an IL-3-dependent mouse mast cell line (PB-3c) after introduction of the v-H-ras oncogene. Tumor progression was characterized by four distinct phenotypes. The first corresponded to immortalized mast cells unresponsive to the oncogenic effect of v-H-ras. The second was expressed in a clonable subpopulation of PB-3c cells and was marked by the competence to form v-H-ras-dependent tumors (immortalized transformation competence). The third was a direct effect of v-H-ras expression on all PB-3c cells and was characterized in vitro by a reduced IL-3 requirement. Upon injection of v-H-ras-expressing, transformation-competent cells into mice, the final, fully malignant phenotype developed with a long latency period and was marked in vitro by independence of exogenous IL-3 and by autocrine IL-3 stimulation. Northern (RNA) blot analysis and an RNase A-T1 protection assay showed that IL-3 production was strictly associated with the tumor phenotype. Two of six tumors showed an alteration at the 5' region of the IL-3 gene. We conclude that v-H-ras required complementation by IL-3 gene rearrangement or an alternate event to generate autocrine mastocytomas.
Mol Cell Biol 1989 Mar
PMID:A v-H-ras-dependent hemopoietic tumor model involving progression from a clonal stage of transformation competence to autocrine interleukin 3 production. 249 44


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