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)

Hyperplasia of mucosal mast cells (MMC) is found in many enteropathies which are caused by T lymphocytes, but their exact role is unknown. In this study we have investigated whether MMC play a part in the immunologically mediated enteropathy which occurs in mice with graft-versus-host reaction (GvHR). There were simultaneous increases in the numbers of jejunal MMC and in the concentrations of mouse intestinal mast cell proteinase both in serum and in the intestine in two separate models of GvHR. Although these changes developed in parallel with the evolving GvHR, there was no correlation between the degree of MMC activation and the severity of the intestinal pathology. In addition, mast cell deficient W/Wv mice developed systemic and intestinal GvHR as severe as their normal congenic littermates, despite a markedly deficient MMC response. We conclude that the role of MMC in enteropathy may be to regulate or repair T lymphocyte mediated immunopathology.
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PMID:Role of mucosal mast cells in intestinal graft-versus-host reaction in the mouse. 210 Nov 24

Information from the NCTR control pathology data base was examined to morphologically classify and correlate the incidence off hyperplastic and neoplastic hematopoietic lesions with age in over 15,000 male and female mice of a variety of strains. Hyperplasia affected lymphoid and reticular cells, erythropoietic and granulopoietic cells, mast cells, plasma cells and megakaryocytes. Neoplastic lesions included lymphocytic lymphoma, mixed cell lymphoma, histiocytic lymphoma, granulocytic leukemia, plasma cell neoplasms and mast cell neoplasms. Most hyperplastic and neoplastic hematopoietic lesions increased wtih age and most were slightly more common in the female than in the male mice.
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PMID:Morphologic classification and correlation of incidence of hyperplastic and neoplastic hematopoietic lesions in mice with age. 726 36

Hyperplasia of airway smooth muscle cells is present in the airways of asthmatic patients and may contribute to the development of the bronchial hyperresponsiveness that occurs in these patients. Because tryptase is an abundant component of mast cell granules and has demonstrated growth-stimulatory effects in other mesenchymal cells (J. Clin. Invest. 1991; 88:493-499), the goal of our study was to determine whether tryptase is a mitogen for airway smooth muscle cells. The mitogenic effects of tryptase were tested in passages 1 through 5 of dog tracheal smooth muscle cells, either by counting smooth muscle cells or by monitoring uptake of bromodeoxyuridine (BrdU) into cellular DNA during S-phase. With respect to its efficacy, at a near maximal concentration (4 nM), tryptase increased cell numbers 2.1 +/- 0.2- or 2.8 +/- 0.6-fold above controls after 2 or 4 days, respectively, and these increases were approximately the same as those induced by platelet-derived growth factor (50 ng/ml) or 10% calf serum. With respect to potency, tryptase caused concentration-dependent increases in BrdU uptake, as detected in an enzyme-linked immunosorbent assay or by counting BrdU-labeled nuclei, with an EC50 of 2 nM. Pretreatment of tryptase with diisopropylfluorophosphate, to reduce markedly its catalytic as a activity as a proteinase, attenuated its growth-stimulated effects by 58 +/- 16%. Tryptase-induced mitogenesis was not a nonspecific effect of all serine proteinases, because thrombin, another proteinase with mitogenicity for fibroblasts, stimulated neither increases in cell counts nor BrdU uptake in our cells. We conclude that tryptase is a potent mitogen for airway smooth muscle cells in culture.
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PMID:Tryptase, the dominant secretory granular protein in human mast cells, is a potent mitogen for cultured dog tracheal smooth muscle cells. 762 90

Dorsal skin responses to a subchronic UVB-irradiation (10kJ/m2/rat /day), were examined in Wistar-derived hypotrichotic WBN/ILA-Ht rats for up to 3 months. Hyperplasia of epidermal cells and hair follicle epithelial cells as well as parakeratosis developed at 1 month and progressed thereafter, resulting in a prominent epidermis thickening and formation of epidermal ingrowths projecting into the dermis. At the same time, the percentage of proliferating cell nuclear antigen (PCNA)-positive epidermal cells significantly increased after I month. In some portions of the hyperplastic epidermis, especially of the epidermal ingrowths, keratinocytes were somewhat pleomorphic and migrated into the dermis. In the upper dermis, edema with capillary congestion, mast cell infiltration and fibroblast proliferation developed at I month, and the intensity of edema and the number of dermal mast cells was most prominent at 3 months. Edema spread to the epidermis, resulting in intercellular edema and subsequent dissociation of epidermal cells. Degeneration of collagen fibers was also detected in the upper dermis, especially beneath the epidermis. In addition, although not significant because of a large individual difference, the serum IgE concentration, showed a tendency to increase after 2 months. The present study clarified the characteristics of the dorsal skin responses to a subchronic UVB-irradiation in rats.
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PMID:Dorsal skin responses to subchronic ultraviolet B (UVB)-irradiation in Wistar-derived hypotrichotic WBN/ILA-Ht rats. 1216 75

Respiratory failure is one of the most serious clinical complications in the course of post-hemorrhagic changes. Cascade-like, systemic inflammatory reaction including the axis: intestines-liver-lung-immune system has a special significance in the pathogenesis of this syndrome. In order to broaden the knowledge of the respiratory insufficiency pathogenesis in hemorrhagic shock, the attempt was made to evaluate quantitatively rat mast cells localized under the pulmonary pleura, around the bronchi, around large vessels and placed in the interalveolar septa. The examinations were conducted on 24 young female Wistar rats, divided into two groups (n=12): (I) sham-operated and (II) shocked. The hemorrhagic shock was evoked by the withdrawal of 25% of the circulating blood. The shock duration was 75 min. The obtained lung sections were stained with toluidine blue and examined in a light microscope. After hemorrhagic shock, sections of lung samples revealed about two-fold increase in mast cell number/mm2 compared to controls. Mast cells were concentrated mostly around the bronchi and blood vessels. Hyperplasia and migration of mast cells may suggest their role in the modulation of inflammatory process causing acute lung injury in the hemorrhagic shock.
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PMID:The evaluation of quantity and distribution of murine pulmonary mast cells in experimental hemorrhagic shock. 1272 93