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)

Acid mucopolysaccharides in mast cell granules were histochemically studied in the lesion of urticaria pigmentosa and in the dermis of normal human skin. Alcian blue and azure A were used to stain mucopolysaccharides. Bromphenol blue was employed for detection of basic proteins. In a further attempt to identify various polyanions, staining was carried out with alcian blue containing various concentrations of electrolytes. Methylation, saponification, and digestion with streptomyces or testicular hyaluronidase, chondroitinase ABC, sialidase, or desoxyribonuclease were also employed. The results obtained are most likely to suggest the presence of hyaluronic acid in mast cell granules.
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PMID:Histochemical demonstration of hyaluronic acid in human dermal mast cells. 5 4

Subcellular fractions containing adrenergic vesicles were obtained from bovine adrenal medulla and splenic nerve, rat and cat heart, and rat spleen. The fractions were washed free from lipids, digested with papain and the mucopolysaccharides (MPSs) then precipitated from the supernatant with ethanolic potassium acetate. The mpsswere identified by several different methods--microelectrophoresis on cellulose acetate in various media, cellulose column chromatography using elution solvents of increasing ionic strength, and treatment with specific enzymes followed by electrophoresis or column chromatography. The MPS precipitate from all the sources investigated contained dermatan sulphate or a dermatan sulphate-chondroitin sulphate hybrid. in addition, the precipitate from rat spleen was found to contain chondroitin sulphate. Heparan sulphate was found in the precipitates from rat heart and spleen and hyaluronic acid in that from bovine splenic nerve. The finding of sulphomucopolysaccharides in the adrenergic vesicles, probably in a complex with protein, raises the question of the functional significance of such complexes. They might, by analogy with the ion-exchange function of the heparin-protein complex in mast cell granules, play a role in the storage and release of the amines.
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PMID:Identification of the mucopolysaccharides in catecholamine-containing subcellular particel fractions from various rat, cat and ox tissues. 13 83

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)
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PMID:A mast cell secretagogue, compound 48/80, prevents the accumulation of hyaluronan in lung tissue injured by ionizing irradiation. 230 75

Tryptase was previously shown to undergo rapid inactivation under physiological conditions unless stabilized by the presence of heparin. The current study shows that increasing the concentration of free tryptase enhances the preservation of enzymic activity, consistent with dissociation of the tetramer, rather than autodegradation, as the mechanism of inactivation. Heparin glycosaminoglycan fragments of Mr greater than 5700 are necessary for complete stabilization of tryptase activity. This stabilizing effect depends upon negative charge density rather than carbohydrate composition. Thus, keratan sulphate or hyaluronic acid were no better than physiological buffer alone; chondroitin monosulphates and heparan sulphate each prolonged the t1/2 about 20-fold over buffer alone; chondroitin sulphate E prolonged the t1/2 69-fold; and dextran sulphate and heparin provided complete stabilization of tryptase activity for 120 min. Poly-D-glutamic acid prolonged the t1/2 55-fold. In each case the loss of tryptase activity followed apparent first-order kinetics. Increasing the NaCl concentration from 0.01 M to 1.0 M increased the stability of free tryptase. In contrast, increasing the NaCl concentration in the presence of stabilizing polysaccharides decreased the stability of tryptase until dissociation of tryptase from each polysaccharide presumably occurred; thereafter tryptase stability increased as did that of free tryptase. The effect of salt concentration on heparin-stabilized tryptase activity (as opposed to stability) was also evaluated. The mast cell proteoglycans heparin and chondroitin sulphate E, by virtue of containing the naturally occurring glycosaminoglycans of highest negative charge density, may play a major role in the regulation of mast cell tryptase activity in vivo.
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PMID:Regulation of human mast cell tryptase. Effects of enzyme concentration, ionic strength and the structure and negative charge density of polysaccharides. 244 72

Since mast cells have previously been shown to be potent modulators of lymphocyte function, the effect of varying concentrations of three mast cell- or basophil- as well as skin ground substance-derived glycosaminoglycans (GAG; heparin, chondroitin sulfate, hyaluronic acid) and of histamine was investigated on rat spleen cell 3H-thymidine incorporation in the absence and presence of mitogens. Modulation proved to be different for the three GAG: chondroitin sulfate was inhibitory and hyaluronic acid enhancing, while heparin exhibited a more complex pattern, with inhibition in control and phytohemagglutinin-stimulated cultures and enhancement in concanavalin A-driven cultures, in parallel to histamine. The data suggest that ground substance GAG as well as mast cell- and basophil-derived mediators in the skin can have a marked and complex modulatory effect on the function of lymphocytes.
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PMID:Modulatory effects of glycosaminoglycans and histamine on lymphocyte mitogenesis. 251 35

Hyaluronan (hyaluronic acid) appears in low concentrations in bronchoalveolar lavage fluid from healthy individuals, while increased amounts have been reported in lavage fluid from patients with interstitial lung diseases and allergic asthma. We have earlier reported a strong correlation between the appearance of lavage fluid mast cells and hyaluronan in patients with sarcoidosis and extrinsic allergic alveolitis. The central role of the mast cell in allergic asthma is well documented. In this study we have investigated if challenge with inhaled histamine, a major mast cell component, could influence the appearance of hyaluronan in bronchoalveolar lavage fluid. A more than twofold increase of hyaluronan was seen 24 h after challenge with histamine. This increase correlated with a less pronounced increase of albumin in lavage fluid. Histamine challenge also induced an increase of mast cells, lymphocytes, and granulocytes in the lavage fluid. The observed histamine effect on the hyaluronan recovery during lavage might be explained by a histamine-mediated leakage of interstitial fluid, rich in hyaluronan, to the alveolar space. Mast cell degranulation of histamine may partly underlie the appearance of increased amounts of hyaluronan in lavage fluid from patients with interstitial lung diseases and allergic asthma.
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PMID:Increased hyaluronan (hyaluronic acid) levels in bronchoalveolar lavage fluid after histamine inhalation. 272 57

Patients (n = 10) at the acute phase of farmer's lung were investigated with chest roentgenography, lung function tests, and bronchoalveolar lavage (BAL) fluid analysis (n = 9). They had diffuse interstitial lung infiltrates and a reduction of the diffusion capacity. The dominating recovered cell types during BAL were lymphocytes; and in two patients, granulocytes. A prominent increase in mast cell numbers was seen in all patients. After avoidance of contact with moldy plant material for four to ten weeks (n = 7), lung function started to improve; and the BAL cell counts, to decrease. At clinical remission six to 14 months later (n = 7), the chest roentgenogram was normal and the diffusion capacity was slightly subnormal. The BAL numbers of mast cells and lymphocytes had further decreased but still remained increased compared with those in the healthy controls. Parallel to the normalization of the lung function and the recovery of BAL fluid cells, the increased BAL fluid concentrations of hyaluronic acid and procollagen III peptide started to decrease. These potential markers of fibroblast activation were significantly related to the mast cell number, but not to the lymphocyte number. The study has demonstrated that pulmonary mastocytosis is a prominent finding in farmer's lung and is related to the disease activity. The observed relationship between pulmonary mastocytosis and biochemical signs of lung fibroblast activation is further evidence to support the hypothesis of a mast cell interaction with lung connective tissue.
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PMID:Bronchoalveolar mastocytosis in farmer's lung is related to the disease activity. 337 20

Hyaluronate (hyaluronic acid), a potential marker for activated pulmonary fibroblasts, appears in increased concentrations in bronchoalveolar lavage fluid from patients with sarcoidosis. The mechanisms underlying fibroblast proliferation are largely unknown but activated alveolar T lymphocytes and macrophages probably play a part; the mast cell is also important for fibroblast proliferation. This study was designed to determine whether there is any association between pulmonary mast cells in lavage fluid, which are known to be increased in patients with sarcoidosis, and signs of pulmonary fibroblast activation. A strong correlation was found between lavage fluid hyaluronate and recovered mast cells (r = 0.72, p less than 0.001). Moreover, mast cell and hyaluronate estimations correlated inversely with lung volume and transfer factor for carbon monoxide, and both indices increased with advancing radiological sarcoid stage. Macrophage and granulocyte counts were normal in lavage fluid from patients with sarcoidosis and were not related to lavage fluid hyaluronate or laboratory signs of the disease in the lungs. Lymphocytes were recovered in increased numbers (p less than 0.001) and were related to the lavage fluid mast cells and hyaluronate. It is concluded that in sarcoidosis release of hyaluronate into the airways is related to the degree of lung disease and to the local inflammatory reaction in the lung as defined by increased numbers of mast cells and lymphocytes in lavage fluid. The findings may reflect a link between the immune system, activation of mast cells, and a pulmonary fibroblast proliferation.
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PMID:Hyaluronic acid in bronchoalveolar lavage fluid in patients with sarcoidosis: relationship to lavage mast cells. 343 82

Hyaluronate and type III procollagen propeptide were assayed in bronchoalveolar lavage (BAL) fluids from patients with sarcoidosis. Levels were significantly elevated suggesting increased rates of synthesis of these connective tissue components in the lung. They were strongly related to each other (p less than 0.001) favoring the idea of a common cellular origin, as a suggestion activated fibroblasts. There was a significant inverse correlation (p less than 0.001) between lavage hyaluronate or procollagen propeptide and the clinical severity of the disease process defined by lung volume, diffusion capacity and pulmonary radiological findings. Correlation of clinical findings with lavage cell profiles was poor except for recovered mast cells (p less than 0.001). Lavage mast cell counts were also closely associated with BAL fluid hyaluronate and procollagen peptide (p less than 0.001). These findings may reflect a link between the mast cell, the activation of fibroblasts, and the progress of connective tissue changes in sarcoid lung.
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PMID:The mast cell and signs of pulmonary fibroblast activation in sarcoidosis. 357 May

The detailed mechanisms which can explain the inherent radiosensitivity of salivary glands remain to be elucidated. Although DNA is the most plausible critical target for the lethal effects of irradiation, interactions with other constituents, such as cell membrane and neuropeptides, have been suggested to cause important physiological changes. Moreover, mast cells seem to be closely linked to radiation-induced pneumonitis. Therefore, in the present study the effects of fractionated irradiation on salivary glands have been assessed with special regard to the appearance of mast cells and its correlation with damage to gland parenchyma. Sprague-Dawley strain rats were unilaterally irradiated to the head and neck with the salivary glands within the radiation field. The irradiation was delivered once daily for 5 days to a total dose of 20, 35 and 45 Gy. The contralateral parotid and submandibular glands served as intra-animal controls and parallel analysis of glands was performed 2, 4, 10 or 180 days following the last radiation treatment. Morphological analysis revealed no obvious changes up to 10 days after the irradiation. At 180 days a radiation dose-dependent loss of gland parenchyma was seen, especially with regard to serious acinar cells in parotid gland and acinar cells and serous CGT (convoluted granular tubule) cells in the submandibular gland. These changes displayed a close correlation with a concomitant dose-dependent enhanced density of mast cells and staining for hyaluronic acid. This cell population seems to conform with the features of the connective tissue mast cell type. The parotid seems to be more sensitive to irradiation than the submandibular gland. Thus, the present results further strengthen the role of and the potential interaction of mast cells with radiation-induced tissue injury and alterations in normal tissue integrity.
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PMID:Increase in mast cells and hyaluronic acid correlates to radiation-induced damage and loss of serous acinar cells in salivary glands: the parotid and submandibular glands differ in radiation sensitivity. 829 28


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