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

We have determined that several chemokines induce mast cell migration in vitro. This directed migration is dependent on the presence of particular extracellular matrix proteins and the activation status of the cells. Mast cell haptotactic responses were observed in response to various chemokines on vitronectin-, laminin-, and fibronectin-coated filters. Unstimulated mast cells were chemoattracted only by monocyte chemotactic protein-1 and RANTES on vitronectin-coated and, to a lesser extent, laminin-coated filters, whereas IgE-activated mast cells migrated in response to monocyte chemotactic protein-1, regulated on activation normal T expressed and secreted, platelet factor-4, and macrophage inflammatory protein-1 alpha on all three matrix proteins. No significant migration was observed on collagen type IV-coated or uncoated filters. Mast cell migration in response to chemokines on extracellular matrices and its enhancement by IgE-dependent activation provide a mechanism by which cells may be drawn to sites of inflammation. Chemokine-induced mast cell recruitment may be particularly relevant in host defense responses to parasitic infections, allergic reactions, Jones-Mote reactions, and in wound healing.
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PMID:Bone marrow-derived murine mast cells migrate, but do not degranulate, in response to chemokines. 753 69

We have evaluated the adhesion of human cutaneous mast cells to several components of the extracellular matrix (plasma fibronectin, laminin, collagen type I and IV) and studied whether these cells express the beta 1 integrins potentially involved in the adhesion to these proteins. Human skin mast cells (5.1 +/- 1.5% pure) spontaneously adhered to fibronectin and laminin (0.1 to 10 micrograms/ml) immobilized on plastic surfaces (e.g., 14 +/- 7.2% and 14 +/- 4.4% adhesion at 10 micrograms/ml, respectively). Similar results were obtained with a 90% pure mast cell preparation. In contrast, cutaneous mast cells did not adhere to collagen type I (1.6 +/- 0.5% adhesion) or type IV (1.2 +/- 0.8% adhesion). Control adhesion in BSA-coated wells was < 5%. Mast cell adhesion to fibronectin was optimal after an incubation period of 60 to 90 min (t1/2 = 28.2 +/- 6.2 min), whereas adhesion to laminin was faster (t1/2 = 10.1 +/- 1.2 min), being nearly optimal after a 15-min incubation period. Human skin mast cell adhesion to fibronectin and laminin was found to be dependent on the presence of divalent cations in the extracellular medium. Dual-color immunofluorescence and flow cytometry were used to evaluate whether human skin mast cells (51.3 +/- 3.9% pure) express beta 1 integrins that may mediate cell adhesion to extracellular matrix proteins. These mast cells were found to express VLA (very late Ag)-3 (75.3 +/- 35.6 specific fluorescence intensity) and, to lesser degree, VLA-4 and VLA-5 receptors (8.0 +/- 2.5 and 6.9 +/- 3.2 specific fluorescence intensity, respectively). In contrast, VLA-1, VLA-2, and VLA-6 integrins were not expressed significantly. mAb to VLA-3, VLA-4, and VLA-5 each inhibited by 70% skin mast cell adhesion to fibronectin. mAb to VLA-3 nearly abolished mast cells adhesion to laminin, whereas anti-VLA-4 and anti-VLA-5 were ineffective. Finally, immunosuppressant cyclosporin A (100 nM) and FK-506 (10 nM) significantly inhibited mast cell adhesion to both fibronectin and laminin (p < 0.05). Our data demonstrate that human skin mast cells spontaneously adhere to fibronectin and laminin, and that this adhesion is mediated by VLA-3, VLA-4, and/or VLA-5 integrins on these cells. Interactions between these beta 1 integrins and extracellular matrix proteins may be involved in perivascular tissue localization of human mast cells in vivo.
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PMID:Human skin mast cells express functional beta 1 integrins that mediate adhesion to extracellular matrix proteins. 753 41

This article describes the etiology, clinical signs, diagnosis, and treatment of various equine nodular diseases. Although of different etiologies, this group of diseases shares a common histologic reaction pattern characterized by infiltration of eosinophils and collagen degeneration. Collagenolytic granuloma, axillary nodular necrosis, unilateral papular dermatosis/eosinophilic folliculitis, amyloidosis, habronemiasis, and mast cell tumors are discussed.
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PMID:Eosinophilic nodular dermatoses. 763 67

Although previous studies have shown that different cells and cell lines of murine origin bind human C1q, suggesting that they display cell surface receptors for C1q, no information is available to indicate whether mouse or human mast cells express C1q receptors. This paper presents the first evidence to show that murine mast cells express specific receptors for C1q. Western blot analysis of cell membrane proteins prepared from a bone marrow-derived mouse cell line using two monospecific polyclonal Abs, one directed against the 60-kDa C1q receptor (C1q-R) that binds to the collagen-like stalk of C1q (cC1q-R) and the other directed against the 33-kDa molecule that binds to the globular "heads" of C1q (gC1q-R), show that both of these receptors are present on these cells. In addition, C1q can induce mast cell migration in a specific and dose-dependent manner. Interestingly, the C1q-induced migratory response was found to be biphasic; the first response peaked at a C1q concentration of 0.1 nM, whereas the second phase peaked at approximately 40 nM. Checkerboard analysis of the mast cell migratory response to C1q showed that the first phase was primarily due to chemotaxis and the second phase was attributable to chemokinesis. Preincubation of C1q with Abs specific for the collagen-like tail of the molecule abolished both its chemotactic and chemokinetic response, whereas heat inactivation of C1q (56 degrees C, 1 h) resulted in 85% abrogation of the chemotactic phase and 42% reduction in the chemokinetic phase. The observed mast cell migratory responses were mediated by cell surface C1q-R(s), as inclusion of a mixture of anti-C1q-R and anti-gC1q-R Abs with the cells inhibited their migratory response toward C1q. However, incubation of cells with various doses of C1q did not result in histamine release. Furthermore, engagement of mast cell C1q-Rs by the ligand C1q induced an antiproliferative response, as coculturing of mast cells with C1q resulted in a specific and dose-dependent decrease in DNA synthesis. These data suggest that C1q-Rs may play a significant role in mast cell function and regulation by providing an important signal through which mast cells can be recruited to inflammatory sites of increased C1q concentration.
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PMID:Murine mast cells express two types of C1q receptors that are involved in the induction of chemotaxis and chemokinesis. 765 Mar 91

We studied the effect of mast cell chymase on the interaction between osteoblasts and extracellular matrix. Chymase was purified from mast cell lysate by anion exchange chromatography. Osteoblasts were isolated from rat calvarias by collagenase digestion. Incubation of osteoblasts with mast cell lysate (40-170 micrograms/ml) or purified chymase (8-32 micrograms/ml) resulted in changes in cell-matrix interaction and cell morphology. Osteoblasts treated with chymase also showed a gradual detachment from the artificial substrata and from the biomatrix (collagen-digested rib fragment). A similar effect of mast cell chymase on the osteoblasts was found in vitro on endosteum of an intact parietal bone. Neutral protease inhibitors abolished the effect of both crude and purified enzyme preparations on the cell-matrix interaction. Mast cell chymase had no effect on osteoblast viability. The effect of enzyme on osteoblast proliferation was studied with lower concentrations of enzyme (0.2 micrograms/ml) in order to avoid cell detachment; there was no effect on either the metaphase index or on the number of cells after 5 days of incubation with chymase. Osteoblast attachment and cell spreading on different matrix proteins (fibronectin, vitronectin, extract of noncollagenous matrix proteins from rat bone) were significantly altered by their pretreatment with chymase. Matrix fibronectin of osteoblasts in culture as well as soluble vitronectin and fibronectin were digested by rat mast cell chymase. Our data suggest that mast cells through action of neutral protease chymase may alter molecules in extracellular matrix that are important in osteoblast adhesion, cell spreading, maintenance of cell morphology, and, most likely, cell function.
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PMID:Interaction of osteoblasts with extracellular matrix: effect of mast cell chymase. 768 44

The extent of mast cell direct involvement in fibrosis is not defined as yet. In the present study we assessed whether long-term co-culture (up to 7 d) of functionally active rat peritoneal mast cells with 3T3 mouse fibroblasts and mass cell activation can affect fibroblast proliferation and collagen production. Co-culture of subconfluent 3T3 fibroblasts with resting mast cells or with mast cells stimulated by alpha IgE (1:35) or repeatedly activated by low concentrations of compound 48/80 (0.25-0.75 microgram/ml) did not alter fibroblast proliferation. However, fibroblast proliferation was increased significantly (100-130%) when mast cells were repeatedly activated with higher concentrations of compound 48/80 (1-3 micrograms/ml). Repeated mast cell activation by compound 48/80 (0.25 microgram/ml) caused a twofold increase in collagen production and this was reduced by 63% by the mast cell stabilizer nedocromil sodium (10(-5) M). At the same time, co-culture of 3T3 fibroblasts with unstimulated or immunologically activated mast cells did not modulate their collagen production. In conclusion, we have demonstrated that mast cell activation, under certain conditions, can enhance significantly 3T3 fibroblast proliferation and collagen production, thus indicating a direct mast cell involvement in the fibrotic processes.
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PMID:Activated mast cells are fibrogenic for 3T3 fibroblasts. 776 71

Endobronchial biopsy and lavage studies have revealed the presence of mast cell, eosinophil, T-lymphocyte and epithelial cell activation in asthma, along with the structural changes of tissue eosinophil infiltration, loss of superficial columnar ciliated epithelial cells and enhanced collagen deposition in the laminar reticularis. As these cellular and structural changes underlie the clinical features of asthma, i.e., symptom expression, variable airflow obstruction and bronchial hyperresponsiveness, and understanding of their induction and regulation is essential to the understanding of the asthmatic process. The acute airway response to allergen has been studied by the technique of local endobronchial allergen challenge with direct airway sampling in asthma. These studies identify allergen-mast cell interaction as the initial airway event, with mediator release inducing bronchoconstriction and enhancing vascular permeability. As preformed cytokines are present in mast cells, cytokine release from this cell population is likely to initiate the process of endothelial cell activation, with upregulation of cell adhesion molecules, and tissue cell recruitment. Subsequent cytokine elaboration from airway macrophages and T-lymphocytes will perpetuate this response while in chronic clinical disease T-lymphocytes, mast cells, matrix tissue, epithelial cells and eosinophils themselves are all likely to contribute to the cytokine pool within the airways and thus to the regulation of inflammatory cell migration and activation.
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PMID:The airway inflammatory response in allergic asthma and its relationship to clinical disease. 779 34

Chronic exposure of human or murine skin to ultraviolet B (UVB) radiation alters dermal extracellular matrix composition and increases the number of mast cells and inflammatory cells. Experiments were designed to test the possible role of UVB-induced tumor necrosis factor-alpha in these photoaging changes based on reports that C3H/HeN, but not C3H/HeJ or Balb/c mice, produce excess TNF-alpha in response to UVB exposure. Pigmented C3H/HeN and C3H/HeJ strains were exposed to a total of 75 J/cm2 of UVB radiation, and unpigmented Balb/c mice were exposed to 19 J/cm2. The UVB-induced increases in collagen, glycosaminoglycans, and neutrophil number were similar or the same in all three strains. The elastin increase was greater in C3H/HeJ than in C3H/HeN mice. The most striking difference between the strains was a 7.7-fold UVB-induced increase in mast cells in C3H/HeN mice compared to no increase in irradiated C3H/HeJ mice and a 2.3-fold increase in Balb/c mice. These results suggest that excess TNF-alpha (or other mediator) produced in C3H/HeN skin (but not C3H/HeJ skin) in response to UVB exposure is involved in the mast cell increase and partial inhibition of elastin increase, but that neither these mediators nor mast cell products are important mediators for the chronic UVB-induced increases in neutrophils, glycosaminoglycans, and collagen. When a possible source of the excess TNF-alpha was investigated, it was found that isolated epidermal cells from all three strains produced increases in TNF-alpha in response to UVB radiation. These results, as well as the previous results showing differences between these strains in UVB-induced effects on cutaneous immune function, are consistent with a model in which UVB-induced mediators from the epidermis stimulate another cell type to produce excess TNF-alpha (and other mediators) in the C3H/HeN but not C3H/HeJ or Balb/c mice.
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PMID:Experimental photoaging in C3H/HeN, C3H/HeJ, and Balb/c mice: comparison of changes in extracellular matrix components and mast cell numbers. 779 17

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

The effect of captopril on the development of hepatic septal fibrosis in a specific experimental model produced by repeated injections of whole pig serum into the peritoneal cavity of rats was studied. The results afforded four basic conclusions. First, the experimental model used seems to be a pure form of septal fibrosis, which depends on active tissue fibroplasia, without hepatocyte necrosis. The fibrotic septa, located between limiting plates of adjacent classic hepatic lobules, and delimiting the classic liver lobule, consisted of collagen fibers infiltrated by eosinophils, mast cells, fat-storing cells (Ito cells), transitional cells and interstitial fibroblasts. Second, the angiotensin-converting enzyme inhibitor captopril attenuated the hepatic fibrosis induced by pig serum administration, as proven by a decrease in hepatic hydroxyproline concentration and histological examination of the liver. Third, this attenuation of hepatic fibrosis might be related, at least in part, to diminished mast cell and eosinophil accumulation in the hepatic tissue. Finally, these data may indicate a novel action of angiotensin-converting enzyme inhibitor in general, and for captopril in particular, as drugs potentially capable of reducing eosinophils in fibrotic processes.
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PMID:Captopril reduces collagen and mast cell and eosinophil accumulation in pig serum-induced rat liver fibrosis. 780 27


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