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)

Products of mast cell degranulation, as well as histamine and serotonin, were added to a Mishell and Dutton preparation for in vitro primary immunisation (induction of IgM antibody formation) to sheep or horse red blood cells. Degranulation products were either obatined beforehand by reacting passively sensitised mast cells with the corresponding antigen (unrelated to or identical with the in vitro immunising antigen) or liberated into the culture medium where mast cells actively sensitised to the in vitro immunising antigen had been added. A 46 to 72 % reduction of direct (IgM) plaque forming cells was observed in all cases. This reduction was prevented by anti-histamine. The responsible mediators were active in the 0 to 24 hour period after antigen introduction. The anaphylactic degranulating antibodies triggering this inhibitory activity were found to be thermolabile in one experiment. An in vivo-induced mast cell degranulation led to a reduced formation of plaque forming cells. The enhancing and immunoregulatory activity of anaphylactic mouse antibodies is therefore tentatively and at least partially attributed to their capacity to degranulate mast cells after contact with the antigen.
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PMID:Regulatory mast cells. I Suppressive action of their products on an in vitro primary immune reaction. 0 41

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

The protease inhibitor alpha-1-antichymotrypsin, which binds to chymotrypsin-like enzymes in a sodium dodecyl sulfate-resistant manner, has been shown recently to be both a normal constituent of brain and an integral component of the neuritic plaques that form in Down's syndrome and Alzheimer's disease. We have now identified in rat brain a Mr 25,000 alpha-1-antichymotrypsin-binding protein classified as a chymotrypsin-like protease by its inhibitor profile and substrate specificity. Release of 125I-labeled breakdown products from bands containing the protease in substrate-linked polyacrylamide gels was examined in parallel with hydrolysis of tetrapeptide chromogenic substrates in vitro to establish conditions under which the Mr 25,000 protease was the only activity being measured in vitro. The protease was completely membrane associated but was extractable using 1 M MgCl2; prior extraction of detergent- and low ionic strength-soluble proteins from membranes was used to increase its specific activity. The formation of sodium dodecyl sulfate-resistant bonds between human alpha-1-antichymotrypsin and the protease (kassoc = 2.9 X 10(6) M-1 s-1) was used to titrate the concentration of free protease solubilized from membranes. The protease cleaved both succinyl-Ala-Ala-Pro-Phe-p-nitroanilide, and methoxy-succinyl-Ala-Ala-Pro-Met-p-nitroanilide, the latter being of interest because cleavage after a methionine residue is predicted to generate the amino terminus of the neuritic plaque component beta-amyloid from its precursor protein. In fact, the solubilized protease degraded 90% of membrane-associated beta-amyloid precursor protein detected by Western blot analysis. The protease was kinetically distinct from both chymotrypsin and cathepsin G in direct comparisons and did not match kinetic values published for the rat mast cell proteases against comparable substrates; we therefore refer to the protease with the descriptive acronym clipsin (for chymotrypsin-like protease). Proteases similar to and potentially identical to clipsin were detected by enzymography in other organs from rat (most notably spleen and adult lung). The enzyme in brain was distinguished by a narrow window of elevated activity surrounding postnatal day 5, which was 12-14-fold higher than levels in day 1 or adult brain. Because independent lines of evidence suggest that a brain chymotrypsin-like protease may be involved in the etiology of Down's syndrome and Alzheimer's disease, clipsin is discussed as a candidate for such a role.
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PMID:Clipsin, a chymotrypsin-like protease in rat brain which is irreversibly inhibited by alpha-1-antichymotrypsin. 230 81

Immune responses of mast cell-deficient WBB6F1-W/Wv mice and their mast cell-sufficient littermates (LM: WBB6F1-W/+, Wv/+ and +/+) were compared. After a single intravenous injection of sheep erythrocytes (SE), polyvinylpyrrolidone or bacterial lipopolysaccharide, the antigen-specific IgM plaque-forming cell (PFC) response of W/Wv mice was similar to or greater than the response of LM mice. When both primary and secondary injections of SE or chicken gamma-globulin were given to mice and antigen-specific IgG PFC responses quantified, the response of W/Wv again was similar to or greater than that of LM mice. Serum titers of antigen-specific IgE were higher in W/Wv than in LM mice after injections of ovalbumin in alum or infections of Nippostrongylus brasiliensis. Ovalbumin-sensitized W/Wv and LM mice developed active systemic anaphylaxis after ovalbumin challenge. The ability of W/Wv mice to be sensitized for and elicit contact sensitivity (CS) reactions was studied using picryl chloride or dinitrofluorobenzene as sensitizing and challenge agents and quantifying 24-hour reactions by change in ear thickness. SE or methylated bovine serum albumin was used to sensitize and challenge mice for delayed-type hypersensitivity (DTH) reactions which were quantified at 24 h by change in foot pad or ear thickness. CS and DTH reactions of W/Wv and LM mice were similar. No evidence of immune deficiency of W/Wv mice was found.
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PMID:Immune response potential of mast cell-deficient W/Wv mice. 351 77

Verruciform xanthoma is an unusual lesion that was initially reported in 1971. Clinically, it is a verrucous, vascular, epithelial plaque or papillomatous growth commonly found on oral or mucosal tissues. Histologically, it is characterized by a verruciform epithelium with abundant parakeratosis and by foam cells occupying the vascularized dermal papillae. This is the second extramucosal verruciform xanthoma reported. Our patient had several unique features. She is the youngest patient described to date, her lesion is the largest reported, and the lesion occurred in an epithelial nevus-type eruption of a phocomelic extremity. Light and electron microscopic studies disclosed abnormal keratinization, mast cell proliferation, and the previously described foam cells. We believe that the verruciform xanthoma in our patient represents part of a reaction to the epithelial nevus occurring in association with a developmental anomaly.
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PMID:Verruciform xanthoma in an epithelial nevus. 681 Jul 62

We have investigated markers of epidermal proliferation and differentiation in terms of keratin expression, the morphology of the cutaneous vasculature, and numbers of cutaneous mast cells, in patients with chronic plaque psoriasis. Using the phenomenon of the 'active edge', we have studied these features in the psoriatic plaque itself, and in the clinically normal active and inactive edges of the same plaque. Our results confirm the anticipated changes in keratin profiles, mast cell numbers and psoriatic morphology of the vasculature within the plaque itself. They further indicate that the vascular changes precede the epidermal and mast cell features at the active edge, and that the inactive edge is inactive for all of these variables. Mediators responsible for the vascular proliferation and elongation must be present in increased amounts at the active edge when compared with the inactive, and include locally produced and circulating factors.
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PMID:Investigations of the 'active' edge of plaque psoriasis: vascular proliferation precedes changes in epidermal keratin. 753 1

ODU Plaque-susceptible rats (ODUS/Odu) exhibit markedly heavy plaque formation in the lower incisors and develop both periodontal pockets and gingivitis after being fed a commercially available powder diet. These rats have been established as an inbred strain. We have demonstrated that the ODUS/Odu are a very suitable experimental model for studying periodontitis. We already reported about the allelic distribution, changes of plaque formation and body weight, biochemical nature, toxic activity, vascular permeability factor and bradykinin inactivating factor of the plaque, histological and immunological studies, the pH in the periodontal pocket, amount of saliva, IgA in the saliva, salivary kallikrein, the relationship between sialic acid in the saliva and the serum, leukocyte functions (chemotaxis and superoxide anion) in ODUS/Odu, histamine, mast cell, free radicals, superoxide dismutase activities in gingiva and gingival nerve fibers with substance P or calcitonin gene-related peptide, and effect of diabetes. Streptozotocin-induced diabetic ODUS/Odu may be a useful tool for studying the pathological mechanisms in the development of periodontal tissue breakdown in diabetes. ODUS/Odu should help to further establish the utility of this strain as a model for experimental periodontal disease.
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PMID:[Experimental periodontitis in rats]. 762 82

Mast cell products, such as histamine, may contribute to the initiation and progression of the atherosclerotic plaque. To determine the relationship that may exist between early atherosclerotic plaques and mast cells we studied the aortas and coronary arteries of 115 young subjects aged 15 to 34 years who had traumatic deaths. Lesions were classified as normal intima, fatty streaks, fibro-fatty plaques, and fibrous plaques. Aortic and coronary artery segments with raised lesions had significantly greater numbers of mast cells in the adventitia (and occasionally intima and outer media) compared with those with a normal intima. In the aortic segments greater numbers of mast cells were located in the dorsal portion (lesion "prone") compared with the ventral half (lesion "resistant") (P < .05). These data support the concept that increased numbers of mast cells are associated with atherosclerosis and suggest a role for mast cell products in the evolution of the atherosclerotic plaque.
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PMID:The association of mast cells and atherosclerosis: a morphologic study of early atherosclerotic lesions in young people. 772 16

The number of mast cells is increased in psoriatic lesions and this is particularly prominent in their early phase. Mediators released by mast cells may interfere with various aspects of cutaneous inflammation and epidermal proliferation. Therefore, the aim of the present investigation was to find out whether a 4-week treatment period with Tiacrilast, a highly potent inhibitor of mast cell degranulation, might have antipsoriatic potential. A total of 31 patients with plaque-type psoriasis were evaluated after treatment with a 3% Tiacrilast hydrogel and hydrogel alone, in a double-blind, placebo-controlled, within-patient comparative study. No statistically significant improvement of the Tiacrilast-treated plaques compared to the hydrogel-treated sites could be demonstrated. Therefore, the present study does not provide evidence of a potential role of mast cell degranulation in the treatment of psoriasis.
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PMID:Inhibitor of the release of mast cell mediators does not improve the psoriatic plaque. 778 22

In this progress report the major pathological results gained from the research program called The Pathological Determinants of Atherosclerosis in Youth (PDAY) are summarized. These results are made possible because of the many unique features of this multicenter study, which are also summarized. The following main accomplishments utilize special quantitative techniques to study cellular, chemical and molecular (genetic) features of the developing plaques in young people. These include for the first time: The greater incidence of early progressive lesions in selective apo E phenotypes. The greater incidence of progressive lesions in black youth with an apo B deletion genotype. The much higher concentration of epitopes of oxidized LDL in smokers than non-smokers. More prevalent macrophages and lymphocytes in the standardized thoracic aortic samples, where lesions progress slowly, than in the abdominal aortic core samples, where lesions are much more likely to become severe. A strong correlation between the mast cell population and the concentration of biogenic amines in the lesions. The location of Lp(a) specific antigens in these developing lesions as compared to apo B. The accumulation of extracellular lipid where progression of lesions is most rapid, with special emphasis on the effects of smoking. The correlation of modulation of the intimal smooth muscle cells with the sites where progression of the plaque is most frequent. Preliminary ultrastructural evidence of intimal platelet and leukocyte adherence and entrance into the intima of the thoracic aorta, where there is likely to be lack of progression of lesions. A review of the recently published biochemical evidence of the correlation of increased lesion cholesterol and collagen content in the abdominal aorta. The continuing studies and their implications are also summarized.
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PMID:New insights into the pathogenesis of atherosclerosis as revealed by PDAY. Pathobiological Determinants of Atherosclerosis in Youth. 780 26


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