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)

Proteases capable of activating procollagenase from gingiva and from fibroblast and macrophage monolayer cultures were harvested from homogenates of canine tumor mast cells. The mast cell proteases lysed casein and Azocoll but not native collagen. In low salt concentrations the enzymes existed at high molecular weight complexes, which were dissociated by increasing the salt concentration above 1.0 M (NaCl, KCl). Gel filtration in 1.4 M KCl separated the protease activity into three peaks, all of which activated procollagenase. Two of the enzymes showed substrate specificities (hydrolysis of p-tosyl-L-arginine methyl ester and benzoyl-tyrosine ethyl ester) and reactive center reactivities similar to pancreatic trypsin and chymotrypsin. Based on gel filtration, apparent molecular weights of 160 000 (p-tosyl-L-arginine methyl ester esterase), 90 000 (main procollagenase activator) and 36 000 benzoyl-tyrosine ethyl ester esterase) were determined. Activation of procollagenase resulted in a 18-20 000 decrease of the molecular weight. The activation was directly related to the amount of activator added within certain limits. Further addition of activator resulted in proteolytic inactivation of collagenase.
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PMID:Activation of fibroblast procollagenase by mast cell proteases. 5 9

Acetic orcein stains formol- and Carnoy-fixed tissues, coloring mast cells, nuclei, basophilic cytoplasm, cerebral corpora amylacea, and cartilage strongly; keratin and erythrocytes moderately; muscle and collagen weakly. Guinea pig Brunner gland and rat colonic goblet cell mucins did not stain. The red nuclear stain contrasts well with the Prussian blue reaction of hemosiderin and the ferric ferricyanide (Turnbull's blue) reaction of enterochromaffin. A weak (0.01%) fast-green FCF stain changes collagen and sometimes smooth muscle to green, without impairing nucleic acid or mast cell staining. Picroindigocarmine gives blue collagen, yellow muscle, and red elastin, nucleic acids and mast cells. Picro-methyl blue tends to override the red nuclear stain. Carnoy fixation is somewhat better for nuclei, formol for basophil cytoplasms.
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PMID:Acetic orcein staining of prefixed tissue sections. 7 35

The activities of four intracellular enzymes of collagen biosynthesis were assayed in freshly isolated rat peritoneal macrophages and mast cells and compared with the same enzymes in freshly isolated chick-embryo tendon cells. The macrophages were found to contain activities of all four enzymes, those of prolyl and lysyl hydroxylase being 7 and 12% respectively of those in the tendon cells when expressed per cell or 3 and 4% when expressed per unit of soluble cell protein. The corresponding values for hydroxylysyl galactosyltransferase and galactosylhydroxylysyl glucosyltransferase activities were about 82 and 68% or 32 and 24% respectively. When the macrophages were incubated in suspension with [(14)C]proline, they synthesized a small but significant amount of non-diffusible hydroxy[(14)C]proline. The synthesis per cell was only about 0.1% of that formed by the tendon cells, and its distribution between the cells and the medium also differed from that in the tendon cells. The hydroxy[(14)C]proline synthesized by the macrophages may be present in the Clq subcomponent of the complement, but its amount was too small to allow any characterization of the protein. All four enzyme activities, and in particular the two hydroxylysyl glycosyltransferase activities, seem to be present in macrophages in a large excess compared with the very low rate of synthesis of hydroxy-proline-containing polypeptide chains. The mast cell extract was found to inhibit all four enzyme activities, but even when corrected for this inhibition, prolyl and lysyl hydroxylase activities in the mast cells were less than 0.08% and the two hydroxylysyl glycosyltransferase activities less than 1% of those in the tendon cells. The intracellular enzyme pattern of collagen biosynthesis in the mast cells is thus completely or virtually completely repressed.
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PMID:Studies on enzymes of collagen biosynthesis and the synthesis of hydroxyproline in macrophages and mast cells. 22 50

Granulation tissues, hypertrophic scars, hypertrophic scars treated with mechanical pressure and mature scars from deep thermal injuries, or equivalent trauma, were examined for the presence and dermal distribution of mast cells. Statistical analyses of mast cell counts indicate that 1) the hypertrophic scar contains significantly greater numbers of mast cells than the other tissues studied. 2) as granulation tissue develops interstitial collagen, mast cells begin to appear, 3) mature scars contain significantly fewer mast cells than hypertrophic scars, 4) based on mast cell data, the effect of pressure therapy is first detected in the upper and middle reticularis of the dermis, and 5) on a mast cell statistical basis mature scar and hypertrophic scar under pressure are indistinguishable.
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PMID:Mast cell analyses in hypertrophic scars, hypertrophic scars treated with pressure and mature scars. 64 83

This study describes the histopathology and ultrastructure of bronchial mucosa in lung biopsies from two children with bronchial asthma in remission, and compares them with lung samples from two children who died in status asthmaticus. Light microscopy of all samples showed changes typical of bronchial asthma, e.g. mucus plugging, goblet cell hyperplasia, 'thickening of bronchial basement membrane', peribronchial smooth muscle hypertrophy and eosinophilic infiltration. Electron microscopy revealed that the mucus plugs consisted of moderately electron-dense floccular material containing degenerate epithelial cells, macrophages and cell fragments. The luminal surfaces of ciliated cells showed cytoplasmic blebs and abnormal cilia. Mast cells in various stages of degranulation were scattered between bronchial epithelial cells. The subepithelial hyaline layer, commonly referred to as "thickened basement membrane", consisted of collagen fibrils in plexiform arrangement. The basement membrane proper appeared intact. These electron microscopic changes, particularly the presence of mast cells and subepithelial collagen deposits, were also found in autopsy samples. This combined light and electron microscopic study shows that marked, possibly irreversible changes may be present in the lungs of patients with severe bronchial asthma, even when they are asymptomatic. These pulmonary changes could be the direct consequence of mast cell activation and the release of various mediators. No evidence of immune complex deposition was found.
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PMID:Ultrastructure of airways in children with asthma. 1240 26

A 57-year-old woman with cutaneous mastocytosis of 23 years duration developed a hyperpigmented abdominal plaque composed of confluent indurated papules that enlarged for a period of 1 year to 12 x 8 cm. Biopsy showed dermal infiltration by closely packed spindle-shaped mast cells, fibroblasts, collagen, and scattered lymphocytes, predominantly T-suppressor cells. Electron microscopy showed close contact between mast cells, fibroblasts, and lymphocytes. Piecemeal mast cell degranulation and extrusion of mast cell granules was seen, with rare mast cell granules in fibroblasts, and collagen fibers in peripheral and perinuclear endoplasmic reticulum of mast cells. the term Fibrous mastocytoma is suggested for this tumor-like dermal fibrosis, possibly induced by lymphokines.
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PMID:Fibrous mastocytoma in a patient with generalized cutaneous mastocytosis. 137 50

Lymph nodes from 21 cases of generalized mastocytosis were studied histologically to confirm or exclude mast cell infiltration, and to investigate their micro-architecture. Mast cell infiltrates were detected in 17 (80%) of the lymph nodes and were found mainly in the medullary cords and sinuses. Diffuse infiltration was seen in 14 cases and focal infiltration in three cases. The following pathological findings were frequently observed: germinal centre hyperplasia (n = 14), which is probably a nonspecific finding; and hyperplasia of small blood vessels, which sometimes resembled high endothelial venules (14), eosinophilia (8), plasmacytosis (7) and collagen fibrosis (6), all of which may well be related to the effects of mediators released by mast cells. Infiltrates of acute or chronic myeloid leukaemia were seen in six lymph nodes. Division of the cases into two prognostically different groups, i.e. systemic mastocytosis, in which the skin lesions of urticaria pigmentosa are present and the prognosis is favourable, and malignant mastocytosis, in which there is no cutaneous involvement and the prognosis is poor, revealed that all six lymph nodes exhibiting leukaemic infiltrates came from the malignant mastocytosis group; eosinophilia, plasmacytosis and fibrosis were seen significantly more often in malignant than in systemic mastocytosis, but blood vessel hyperplasia and germinal centre hyperplasia were encountered with the same high frequency in both groups; and mast cell atypia tended to be more pronounced in malignant mastocytosis; this diagnosis could therefore easily be missed without naphthol AS-D chloroacetate esterase staining.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lymph node findings in generalized mastocytosis. 145 27

The ultrastructure of nasal polyps from cystic fibrosis (CF) patients was compared with non-CF nasal polyps in this study. Morphometric analysis showed that CF nasal polyps contained greater numbers of mast cells, endothelial cells, lymphocytes, and plasma cells compared with the non-CF specimens. Morphologic evidence of degranulation was seen in approximately 30 per cent of the CF mast cells but was not observed in the non-CF mast cells. Increased numbers of small granules, vacuolated granules, and lipid bodies were noted in the CF compared with the non-CF nasal polyp mast cells. Also observed was a decrease in collagen in the extracellular space of the CF nasal polyps compared with the non-CF specimens. Although eosinophils were observed in the non-CF nasal polyp tissue, these leukocytes were absent in the CF nasal polyps. These data indicate that striking morphologic differences exist between CF and non-CF nasal polyps with mast cell degranulation, a salient feature of CF specimens.
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PMID:Degranulation of cystic fibrosis nasal polyp mast cells. 151 93

The inflammatory basis of asthma is now beyond dispute and even mild asthmatics exhibit mast cell degranulation, eosinophil infiltration and increases in mononuclear cells in airway mucosal biopsies. The chronic nature of this endobronchial inflammation may cause damage to ciliated epithelium, which, coupled with laying down of cross-linked collagen within the airway wall, leads to partly irreversible airway obstruction. Corticosteroids, which are potent anti-inflammatory agents, decrease bronchial hyperresponsiveness and the clinical manifestations of asthma. Although inhaled corticosteroids produce fewer side-effects, the use of low-dose (10 mg or less) oral treatment may be recommended for patients unable financially to afford inhaled corticosteroids or who are unable to use them effectively. Other anti-inflammatory drugs, including methotrexate, cyclosporin and the newer leukotriene inhibitors, are not yet in general use and may provide new pharmacological approaches to the treatment of asthma in the near future. In all but the mildest asthma, strategies aimed at preventing and decreasing bronchial inflammation should be the primary aim of treatment. The physician should refrain from prescribing only beta 2-agonists to new asthmatics and patients must be educated to increase understanding of the benefits of preventive rather than symptomatic forms of treatment for this chronic disease.
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PMID:Anti-inflammatory strategies for the treatment of asthma. 157 May 78

We studied the role of atopy, as defined by positive skin tests to common inhalant allergens, in allergic bronchial inflammation. Endobronchial biopsies were taken via the fibreoptic bronchoscope in 13 symptomatic atopic asthmatics, 10 atopic nonasthmatics, and 7 normals. The numbers of mast cells, identified in the submucosa by immunohistochemistry using the AA1 monoclonal antibody against tryptase, were no different between the three groups, but electron microscopy showed that mast cell degranulation, although less marked in atopic nonasthmatics, was a feature of atopy in general. The numbers of eosinophils, identified by immunohistochemical staining using the monoclonal anti-eosinophil cationic protein antibody, EG2, were greatest in the asthmatics, low or absent in the normals and intermediate in the atopic nonasthmatics. In both atopic groups eosinophils showed ultrastructural features of degranulation. Measurements of subepithelial basement membrane thickness on electron micrographs showed that the collagen layer was thickest in the asthmatics, intermediate in the atopic nonasthmatics and thinnest in the normals. The results suggest that airways eosinophilia and degranulation of eosinophils and mast cells, as well as increased subepithelial collagen deposition, are a feature of atopy in general and suggest that the degree of change may determine the clinical expression of this immune disorder.
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PMID:Bronchial mucosal manifestations of atopy: a comparison of markers of inflammation between atopic asthmatics, atopic nonasthmatics and healthy controls. 161 55


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