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)

There are both similarities and differences between chronic graft-versus-host disease (GVHD) and scleroderma. The similarities include chronic fibrosis, immunological (autoimmune) abnormalities and perhaps mast cell involvement. The differences include the type of collagen laid down and its precise location, and the distribution of organ involvement. However, a common thread appears to be an immunologically-mediated fibrotic process, involving T cells, fibroblasts and perhaps mast cells. For this reason, we believe that important insights for scleroderma will come from the study of GVHD, in spite of the differences between the two syndromes. Indeed, it would not be expected that GVHD and scleroderma would be identical.
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PMID:Is graft-versus-host disease a reliable model for scleroderma? 357 48

Liver cirrhosis was induced by consecutive CCl4-treatment of rats (0.5 ml/kg, s.c., 2 times/week) to investigate the effect of TRQ on the acceleration of fibrosis in the liver. An increase of hydroxyproline content in the liver of rats began 12 weeks after the CCl4 treatment and a 1.9-fold increase was observed at week 14 compared with non-CCl4 treated rats. Histamine in the liver increased about 2 times at week 14. Increased numbers of mast cells were seen in the area of proliferated collagen fiber in the liver under microscopic observation, and also a good correlation was recognized between the number of mast cells and the progression of fibrosis. An administration of TRQ to the rats for 2 weeks from week 13 resulted in significant suppression of both the increase in hydroxyproline and histamine in the liver dose-dependently compared with the CCl4 control group. Both progression of collagen and increase in mast cell numbers were also suppressed by TRQ dose-dependently under histopathological observation; at the same time the decrease in mast cells was recognized to correspond to the decrease in hydroxyproline and histamine in the liver. Thus, it was suggested that increased mast cells participated in the biosynthesis of collagen. Though the elevated serum transaminases, alkaline phosphatase and leucine amino peptidase were also suppressed by TRQ administration, the protein biosynthesis activity of the liver and lowered serum total cholesterol were not improved as much as the other parameters. From these results, it was shown that TRQ was especially and remarkably effective in suppressing the acceleration of fibrosis, and one of the pharmacological mechanisms of this action may be ascribed to the inhibitory effect of TRQ on the activation of mast cells by some stimulants.
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PMID:[Suppressive effect of tritoqualine (TRQ) on the acceleration of fibrosis in the liver]. 371 Mar 12

Recent investigations revealed that basophil-mast cells were related to the hemopoietic system. Strikingly, murine bone marrow showed a singular paucity in cells with basophil-mast features; moreover in clonogenic assays (methylcellulose, agarose) bone marrow was found to be manifestly poor in basophil-mast progenitor cells. Our work brought to light several new facts concerning the culture and differentiation of this cell type: 1 degree pure and mixed mast clones can be derived in large numbers from bone marrow, provided progenitors are cultured in collagen matrix. Up to 1,382 hemopoietic clones were analysed in situ after staining: 30% contained mast cells (34 per 10(5) cells), thus the basophil-mast lineage was one of the most frequent. We concluded that other cloning media were noticeably nonoptimal for the growth and/or maturation of mast cells. We suggested that collagen and the molecular edifices derived from it, both found in variable amounts in the natural mast environments, should play essential roles in mast phenotype expression. 2 Degrees cholera toxin (CT) selectively eradicated nonmast progenies: mast progenitors and mast progenies were resistant. In this way, pure and rapidly expanding mast cell clones were obtained at a frequency never reported before. CT possibly acts both directly, as a stimulator of mast cell proliferation, or indirectly on marrow subpopulations which repress basophil-mast cell growth and maturation. In vitro culture conditions, specifically designed for basophil-mast lineage, should prove of interest in the search for an unifying hypothesis concerning the multiple forms of mast cells found in various tissues.
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PMID:Murine basophil-mast differentiation: toward optimal conditions for selective growth and maturation of basophil-mast or allied cells. 377 53

Numbers of mast cells were quantitated in the lesions of diffuse scleroderma and morphea. Mast cells increased and then decreased in number in the papillary dermis of diffuse scleroderma. No significant change of mast cell numbers was noted in the reticular dermis. Mast cells increased in the papillary dermis with fine collagen bundles (grade 2 skin of scleroderma) and decreased in the papillary dermis with homogeneous collagen bundles (grade 3 skin of scleroderma). The total number of cells increased in the papillary dermis of grade 1 and 2 skin of scleroderma and decreased in the grade 3 skin of scleroderma. In morphea a reduced number of mast cells was noted in grade 3 lesions. It is suggested that mast cells play an important role in fibrotic process of scleroderma skin.
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PMID:Mast cell numbers in diffuse scleroderma. 381 93

Dermal collagen deposition is the hallmark of the early indurative phase of progressive systemic sclerosis (scleroderma). This process, however, tends to remit in late stages of the disease. Because mast cells are believed to participate in the development of fibrotic processes, we measured the density of the cutaneous mast cell population in clinically involved and uninvolved skin of a group of patients with scleroderma. Mast cell counts in clinically involved skin of patients with early stages of scleroderma (111 +/- 28 [SD] cells/mm2) were significantly greater than those in clinically uninvolved skin of the same patients (58 +/- 26 cells/mm2) and also greater than those of normal controls (50 +/- 14 cells/mm2). Mast cell counts in clinically involved and uninvolved skin of patients with late scleroderma were normal. When mast cell density was analyzed by depth of dermis, an 85% increase was noted in involved papillary dermis and a 152% increase in involved reticular dermis in patients with early scleroderma when compared with densities in controls. These results suggest that mast cells may be important in the pathogenesis of the early cutaneous lesions of progressive systemic sclerosis, perhaps by promoting fibrosis.
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PMID:Increased dermal mast cell populations in progressive systemic sclerosis: a link in chronic fibrosis? 396 56

A single intraperitoneal injection of Ascaris cuticle caused a local eosinophilia with peak levels at 2 wk after injection. Mast cells reduced in number and size at 1 wk were found in increased numbers at 3 wk. Injection of a collagen-poor fraction of cuticle known as "cuticlin" resulted in a diminished eosinophil and mast cell response compared with injection of whole cuticle. Precipitating antibodies to soluble Ascaris cuticle collagen were detected in the serum and peritoneal fluid from day 5 onward. It is proposed that the eosinophilia and mast cell hyperplasia are the result of immunization of the animal to an antigen present in Ascaris collagen and rendered soluble by the action of mononuclear phagocytes. The eosinophil and mast cell response to Ascaris cuticle mimicked the response in connective tissue to living nematode parasites. It is concluded that the cuticle of nematode parasites may be responsible for eosinophilia and mast cell hyperplasia in the host.
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PMID:Eosinophilia, mast cell hyperplasia and antibody production in rats following an intraperitoneal injection of Ascaris cuticle including in-vitro studies of immune eosinophil granule lysis. 400 Jul 8

We explored the pathologic changes in the skin of mice undergoing a chronic graft-versus-host (GVH) reaction. In rodents and in man, chronic GVH includes the deposition of excess collagen in the skin-a reaction which resembles idiopathic scleroderma. GVH disease across minor histocompatibility barriers was produced by injecting B10.D2 cells into irradiated BALB/c mice. These strains are identical at the H-2 and Mls loci but differ in minor histocompatibility antigens. Control BALB/c mice received irradiation and BALB/c cells. Serial skin biopsies were taken and studied for histological changes characteristic of chronic GVHD, for mast cell density, and for the deposition of immunoreactants. GVHD was produced in B10.D2----BALB/c mice as measured by body weight loss and the production of skin changes including dermal fibrosis, loss of fat and appendages, and a mononuclear cell infiltrate. Dermal mast cells, assessed by toluidine blue staining, were normal at Day 11, but had disappeared by Days 21-63 and returned to normal by Day 104. Immunoglobulins IgG, IgA, and IgM appeared at the dermo-epidermal junction and along the basement membrane zone of hair follicles. This deposition was maximal at Day 42 and waned thereafter. Thus the appearance of immunoglobulins in the skin was maximal when mast cell staining was minimal. The changes in this GVHD model leading to a scleroderma-like picture in the skin are compatible with an immune etiology for the fibrosis. Vasodilation following liberation of mast cell mediators would facilitate the deposition of immunoglobulins. The disappearance of mast cell staining may be caused by extensive degranulation. We postulate an interaction between GVHD-activated T cells, mast cell stimulation, fibroblast activation, and fibrosis.
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PMID:Chronic graft-versus-host disease as a model for scleroderma. II. Mast cell depletion with deposition of immunoglobulins in the skin and fibrosis. 401 62

In sympathectomized cats the innervation of the Achilles tendon by fine afferent nerve fibers was studied with semithin and ultrathin sections. Several different types of sensory endings of group III and group IV nerve fibers were identified. Of the five different types of endings in the group III range (T III endings), two are located within vessel walls. One of them ends in the circumference of the venous vessels (T III/VV). Its lanceolate terminals have characteristic receptor areas at their edges. The second type ends in the adventitia of lymphatic vessels (T III/LV). Its receptive areas are scattered along their terminal course. Two further group III endings ramify within the connective tissue compartments of the vessel-nerve-fascicles of the peritenonium externum and internum. One type is tightly surrounded by collagen fibrils (T III/PTic); the other terminates between the collagen fiber bundles (T III/PTgc). The latter arrangement recalls the ultrastructural relation between nerve terminals and collagen tissue in Golgi tendon organs. The fifth type innervates the endoneural connective tissue of small nerve fiber bundles (T III/EN). At least some of them come into close contact with bundles of collagen fibers which penetrate the perineural sheath to terminate within the endoneurium. The endings of group IV afferents (T IV endings) show a striking topographic relationship to the blood and lymphatic vessels of all connective tissue compartments of the Achilles tendon. They form penicillate endings which may contain granulated vesicles. In any event, they can easily be discriminated from the T III endings in the vessel walls. In close neighborhood to Remak bundles, a cell has been regularly found which fulfilled all ultrastructural criteria for mast cells. But this cell is not a mast cell proper because it is surrounded by a basal lamina (pseudo mast cell).
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PMID:Sensory innervation of the Achilles tendon by group III and IV afferent fibers. 405 Nov 91

1. The subunit structure of rabbit subcomponent C1q was examined in a previous publication (Reid et al., 1972). The present paper describes some aspects of the structure of the polypeptide chains derived from the molecule. 2. The three polypeptide chains, produced by performic oxidation, of rabbit subcomponent C1q were isolated by ion-exchange chromatography in 8m-urea on DEAE-cellulose. 3. Each chain was found to contain 15-18% glycine and significant amounts of the amino acids hydroxyproline and hydroxylysine. 4. By means of collagenase digestion it was shown that all three chains of rabbit subcomponent C1q contain collagen-like sequences of amino acids which constitute about 40% of each chain. 5. By use of carboxypeptidase A it was established, indirectly, that the collagen-like sequences, in one of the chains, are probably located near, or at, the N-terminal end of the chain. 6. Collagenase digestion and heating at 52 degrees C (but not at 49 degrees C) caused rapid loss of native rabbit subcomponent C1q haemolytic activity.
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PMID:Studies on the structure and activity of rabbit Clq (a subcomponent of the first component of complement). 437 40

The distributions of laminin, fibronectin, and interstitial collagen type III have been investigated in a series of 60 soft tissue tumours by immunochemistry. Positive laminin staining was seen in sites predicted by the distribution of ultrastructurally visible basal lamina. Pericellular laminin was present in all benign tumours of Schwann cell and smooth muscle origin examined, in the two malignant Schwannomas examined, and in six of 13 leiomyosarcomas. It was also evident around nests of cells in an alveolar soft part sarcoma and around malignant endothelial cells in an angiosarcoma. In fibroblastic and fibrohistiocytic tumours it was found only in blood vessel walls. The results of laminin staining led to revision of the original histopathological diagnosis in seven of the 60 cases studied. Fibronectin was abundant in the stroma of most neoplasms, both benign and malignant. It was also found in a distribution parallel to that of laminin. In some tumours this was clearly distinguishable from the distribution of interstitial collagen. Intracellular fibronectin was shown consistently only in mast cell granules. Its demonstration in synovial cells, fibroblasts, and histiocytes was more variable. Interstitial collagen type II had the most irregular distribution of the three proteins. It was as plentiful in tumours of smooth muscle origin as in tumours of fibroblastic origin, but was scanty in fibrous histiocytomas. Its distribution appeared similar to that of laminin and fibronectin in leiomyomas, but differed from these two proteins in Schwann cell tumours and other neoplasms. In one leiomyosarcoma fibronectin, laminin, and type III collagen appeared to be lost concomitantly from tumour cell peripheries.
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PMID:Distribution of laminin, fibronectin, and interstitial collagen type III in soft tissue tumours. 608 88


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