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

An integrated view of the pathogenesis of scleroderma should include vascular, immunologic, and fibrotic processes. This review introduces the mast cell into this picture, emphasizing recent knowledge gained from a study of experimental chronic graft-vs-host disease and scleroderma itself. In both of these situations, increased mast cell activity occurs. A link between the activation of both endothelial cells and fibroblasts may be provided by the family of heparin-binding growth factors. These cytokines are produced by many cells and are bound, protected, and enhanced by heparin, which may be provided by the activated mast cells. These and other growth factors may be responsible for endothelial proliferation and excess collagen production by fibroblasts. This enlarged schema should provide additional points for therapeutic intervention in scleroderma.
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PMID:On scleroderma. Mast cells, endothelial cells, and fibroblasts. 229 59

A 77-year-old woman had variceal bleeding related to systemic mastocytosis. Physical examination revealed minimal ascites and mild hepatomegaly noted 11 years before. Liver function tests were nearly normal. Because of early recurrent bleeding, a mesocaval shunt was performed. Wedged liver biopsy showed a moderate fibrosis of portal tracts and massive mast cell infiltration within portal tracts and sinusoids. Perisinusoidal collagen deposition was demonstrated ultrastructurally. We suggest that systemic mastocytosis be added to the list of diseases related portal hypertension with perisinusoidal fibrosis. As there is currently no specific treatment, a portocaval shunt should be discussed.
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PMID:[Systemic mastocytosis disclosed by rupture of esophageal varices]. 268 73

When mouse bone marrow-derived mast cells (BMMC) are cocultured with a confluent layer of mouse 3T3 fibroblasts in the presence of WEHI-3-conditioned medium, the mast cells undergo a phenotypic change toward that of a connective tissue mast cell, and the fibroblasts increase their synthesis of globopentaosylceramide. We now demonstrate that fibroblasts lose their contact inhibition and multiply such that by the 2nd and the 4th wk of coculture there are, respectively, approximately four-fold and six-fold more fibroblasts than in the cultures that are not exposed to BMMC. This in vitro increase in the number of fibroblasts is dependent on the number of mast cells (over the range of 6 x 10(4) to 1 x 10(6) BMMC/culture) initially seeded with the fibroblasts and on the concentration of WEHI-3-conditioned medium present during the coculture. That the fibroblasts also multiply in BMMC/fibroblast cocultures exposed to synthetic IL-3 or to purified IL-3 indicates that IL-3 is a component in WEHI-3-conditioned medium that induces mast cells to produce the fibroblast growth factor. The number of fibroblasts does not increase if fibroblasts are exposed to lysates of BMMC, or to BMMC-derived conditioned medium, or if the two cell types are separated from one another during the coculture with a 3-microns filter or a 0.4-microns filter. Thus, IL-3-activated BMMC must be in proximity to fibroblasts to induce them to multiply. Because of their increased numbers per culture dish, total fibroblasts that were cocultured with mast cells synthesized approximately two-fold more 35S-labeled proteoglycans, incorporated approximately 3-fold more [3H] proline into collagenase-sensitive proteins, and had substantially more alpha 2(I) collagen mRNA than fibroblasts that were maintained in the absence of mast cells. These is vitro studies reveal a sequence by which IL-3-activated mast cells may play a role in the induction of fibrosis.
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PMID:Regulation of the growth rate of mouse fibroblasts by IL-3-activated mouse bone marrow-derived mast cells. 278 27

Macrophages possess a number of surface receptors that are capable of mediating the internalization of lipoproteins. The low-density lipoprotein (LDL) receptor of human monocyte macrophages recognizes apolipoprotein B-100 and apolipoprotein E and is rapidly regulated in response to changes in intracellular cholesterol levels. In contrast, in J774 macrophages LDL receptor regulation is defective and LDL can cause massive cholesterol accumulation. The beta migrating very low density lipoprotein (beta-VLDL) receptor is poorly regulated by cellular cholesterol concentrations, readily recognizes apolipoprotein E, poorly recognizes apolipoprotein B-100, and is immunologically related to the LDL receptor. The scavenger receptor (acetyl-LDL receptor) appears to have a molecular weight of 250,000 and is not regulated by cellular cholesterol levels. This receptor recognizes LDL that has been chemically or biologically altered. LDL complexes can also enter macrophages and cause cholesterol accumulation. Examples of such complexes are LDL-dextran sulphate complexes, LDL-proteoglycan aggregates, LDL-mast cell granule complexes, LDL-heparin-fibronectin-denatured collagen complexes, and LDL-antibody complexes. The entry of lipoprotein into macrophages by a pathway that is poorly regulated or is not regulated by cellular cholesterol concentrations appears to be a prerequisite for the formation of arterial foam cells.
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PMID:Macrophage lipoprotein receptors. 285 2

We have undertaken detailed cellular and ultrastructural examination of bronchial biopsies and bronchial lavage fluid from allergic asthmatic patients in order to determine the nature and degree of the inflammatory processes in mild allergic asthma. Eight atopic asthmatic patients (mean PC20 histamine, 0.90 mg/ml) and four nonasthmatic control subjects underwent fiberoptic bronchoscopy. All asthmatic subjects were clinically stable for 2 wk prior to bronchoscopy and required either no treatment or inhaled albuterol alone. A single 50-ml bronchial wash was undertaken, followed by endobronchial biopsy of subcarinae. These procedures were repeated in the asthmatic subjects 18 h after bronchial provocation with allergen or methacholine. Subsequently, all subjects underwent bronchial reactivity testing with inhaled histamine. The clinical and physiologic data were not revealed to the pathologist interpreting the specimens. The asthmatic subjects shed a significantly greater number of epithelial cells into the lavage fluid than did the nonasthmatic subjects (7.23 versus 1.48 x 10(4)/ml, p = 0.048). There was a statistically significant inverse correlation between the lavage epithelial cell count and bronchial reactivity (rho = -0.64, p = 0.03). In the asthmatic subjects, but not in the control subjects, there was extensive deposition of collagen beneath the epithelial basement membrane, mast cell degranulation, and mucosal infiltration by eosinophils, which exhibited morphologic evidence of activation. Eosinophils, monocytes, and platelets were found in contact with the vascular endothelium, with emigration of eosinophils and monocytes in the asthmatic subjects. These changes were found irrespective of bronchial challenge with allergen. We conclude that allergic asthma is accompanied by extensive inflammatory changes in the airways, even in mild clinical and subclinical disease.
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PMID:Cellular events in the bronchi in mild asthma and after bronchial provocation. 292 80

The testicular connective tissue of patients with alcoholic and non-alcoholic cirrhosis was studied by Picrosirius staining for collagen fibres and electron microscopy, and then compared with the connective tissue of normal testes. Under polarized light, the interstitial connective tissue in the testes of patients with alcoholic and non-alcoholic cirrhosis exhibited a green birefringence which did not appear in normal testes, and the orange birefringence characteristic of the tunica propria in the testes of both cirrhotic and normal males was less developed in cirrhosis. This suggests that a connective tissue, consisting of smaller and less ordered collagen fibre bundles than those in the tunica propria is formed in the testicular interstitium of cirrhotic males, and the collagen fibre bundles of the tunica propria are less developed than in normal testes. The appearance of connective tissue was associated with a decrease in the number of mast cells in the testes of cirrhotic males suggesting the involvement of mast cells in the synthesis, packing, and organization of collagen fibres. The cause of the decrease in mast cell numbers may be related to hormone alterations, in particular testosterone deficiency.
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PMID:Changes in the connective tissue and decrease in the number of mast cells in the testes of men with alcoholic and non-alcoholic cirrhosis. 310 54

Mast cells are in close contact with other cells in neurofibromatosis, e.g. neural cells and fibroblasts. Secretory products of mast cells may be important in the regulation of collagen synthesis by fibroblasts and Schwann cells. Newer methods of detecting mast cells by avidin staining of granules and localization of membrane Fc receptors for IgE have been exploited in at least one experimental model of fibrosis (murine chronic graft-versus-host disease). Such approaches should help in understanding parameters involved in modulation of cell growth in neurofibromas. Future directions for the study of cellular dynamics in neurofibromas should include detection of activated (degranulated) mast cells, Schwann cells and effects of mast cell products on collagen gene expression.
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PMID:Mast cells and neurofibromatosis. 315 31

Descriptions of actinically damaged human dermis have focused on the late stages of elastotic degeneration. This has diverted attention from preceding events, which are important for understanding the sequence of pathologic changes that culminate in the deranged fibrous structures of elastotic dermis. We studied specimens from the back of the necks (exposed) and inner arms (unexposed) of 24 individuals, aged 35-84 yr, by light and transmission electron microscopy. Intense sunlight exposure was common to all. A previously undescribed finding was the presence of a perivenular, histiocytic-lymphocytic infiltrate in which numerous mast cells, often in close apposition to fibroblasts, were observed. We have termed this "chronic heliodermatitis." We postulate that mast cell-derived mediators in conjunction with enzymes released by the infiltrating cells lead to breakdown of elastic and collagen fibers.
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PMID:Chronic heliodermatitis: a morphologic evaluation of chronic actinic dermal damage with emphasis on the role of mast cells. 334 56

Intestinal anaphylaxis is associated with disturbances in gut function that are antigen-specific and dependent on mast cell degranulation. Using an animal model of intestinal anaphylaxis, we have correlated alterations in water and electrolyte transport, associated with intraluminal challenge, with specific intestinal mucosal mast cell degranulation by following systemic as well as local release of rat mast cell protease II. This protease is specific for intestinal mucosal mast cells and is known to selectively attack type IV collagen, which is found in basement membranes. Intraluminal antigen challenge in sensitized animals dramatically increased serum and intraluminal levels of rat mast cell protease II. Serum levels continued to rise throughout the duration of antigen challenge. Although light microscopy of challenged intestine demonstrated little distortion of mucosal architecture, ultrastructural examination revealed significant disruption to the basement membrane and underlying collagenous matrix of the intestinal mucosa. Our findings indicate that during mucosal immunoglobulin E-mediated reactions, rat mast cell protease II is released and is associated with ultrastructural changes in the intestinal mucosa. The systemic appearance of this specific protease provides a serum marker of intestinal anaphylaxis.
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PMID:Mast cell protease release and mucosal ultrastructure during intestinal anaphylaxis in the rat. 342 67

One hundred and three teeth with chronic pulpitis, twelve chronic periapical lesions and eleven oral various soft tissue biopsies were used to discuss the presence, the anatomy and function of mast cells. The mast cell induces veinules dilatation during the early phase of inflammation by histamine release, collagen lysis, bone resorption and epithelium proliferation. It can be observed in every chronic lesion and plays a part in both humoral and cellular immunological phenomenons. A more accurate knowledge of its biochemical actions could help in understanding the mechanism of pain in certain clinical dental crisis.
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PMID:[Mastocytes and the oral cavity. Anatomy and function]. 346 Jan 57


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