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

The present study has extended histochemical and functional investigations into rat mast cell heterogeneity using isolated mast cells from four connective tissue locations; the peritoneum, mesentery, lung and skin. On histological examination, mast cells from these locations displayed a range of phenotypes following formalin fixation and staining with Alcian blue/safranin O, suggesting the existence of both chondroitin sulphate and heparin proteoglycans in varying proportions in these cell types. Functional studies using the structurally diverse polycationic secretagogues, compound 48/80, the polyamino acids, polymyxin B, substance P, ACTH1-24, mastoparan, protamine sulphate, histone, d-tubocurarine and ranitidine confirmed the existence of such phenotypic gradation. This investigation highlights the inappropriate usage of the terms CTMC and MMC which represent two phenotypic extremes between which a gradation of phenotypes clearly exists.
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PMID:Mast cell heterogeneity: evidence that mast cells isolated from various connective tissue locations in the rat display markedly graded phenotypes. 137 40

Rat peritoneal mast cells (RPMC) and rat basophilic leukemia (RBL) cells are representative of connective tissue-type (CTMC) and mucosal-type (MMC) mast cells, respectively. Using polyethylene glycol, we have fused RPMC with 6-thioguanine resistant, HAT (hypoxanthine, aminopterin, thymidine) sensitive RBL-CA10.7 or RBL-CK2 cells, yielding several hybrid rat mast cell lines (HRMC). The hybridomas exhibited different size and cytoplasmic granularity when compared with parental cell lines. Analysis of both high (Fc epsilon RI) and low affinity (Fc epsilon RL) receptors for IgE revealed that the hybrid lines had more variable receptor patterns than the parent lines. Three hybridoma lines were chosen for further study. Differential histochemical staining with alcian blue and safranin O dyes indicated the hybrids to be predominantly of the MMC type: however, a few cells of one of these uncloned hybridomas were found to be of the CTMC type. Attempts to isolate the CTMC hybridomas yielded one culture which was predominantly of the CTMC phenotype and in a number of other cultures, cells were found expressing simultaneously both the CTMC and the MMC phenotype. After 3 weeks in culture, however, all hybridomas, including those which were cloned further, expressed only the MMC histochemical phenotype. This was found to correlate with the presence of rat mast cell protease II (RMCPII) and the absence of RMCPI in all hybridomas, as detected by Western blot analysis. In addition, the histamine content of all cells was significantly lower than that of the parent RPMC. Most hybrid mast cells expressed both Fc epsilon RI and Fc epsilon RL which in some cases exhibited significant variations in the Mr. These results indicate that somatic cell hybrids expressing the MMC and CTMC phenotype can be produced by the fusion of RBL and RPMC. The CTMC phenotype, however, is unstable, and possible reasons for this are discussed.
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PMID:Establishment and characterization of hybrid rat mast cells. 182 10

A variety of mast cell degranulating agents have previously been shown to induce mast cell hyperplasia in adult rats. In neonates 2.5 S nerve growth factor (NGF) induces a hyperplasia of both mucosal and connective tissue mast cells (MMC and CTMC). We have examined the role of the potent mast cell degranulating properties of NGF on its ability to induce mast cell hyperplasia. Administration of NGF in combination with the mast cell stabilizing agent disodium cromoglycate was found to abrogate the CTMC hyperplasia induced by NGF alone. Treatment of neonatal rats with the alternate degranulating agent compound 48/80 was found to induce a limited CTMC but not a MMC hyperplasia. A supernatant obtained by degranulating purified adult rat peritoneal mast cells with anti-IgE was found to induce hyperplasia of the CTMC population similar to that observed with NGF administration. However, this degranulation product supernatant only induced a limited MMC hyperplasia as judged by RMCP II content of the tissues. These results suggest that NGF has dual action inducing mast cell hyperplasia; CTMC hyperplasia being dependent on the ability of NGF to degranulate mast cells. MMC hyperplasia induced by NGF is independent of CTMC degranulation. Degranulation products from peritoneal mast cells act to increase both MMC and CTMC populations in the neonate. These data suggest that the CTMC population may be regulated by an autocrine positive feedback mechanism in vivo.
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PMID:The role of mast cell degranulation products in mast cell hyperplasia. I. Mechanism of action of nerve growth factor. 210 55

A formalin fixative and a formalin-free fixative were used to study mast cells in the small intestine of conventional, gnotobiotic and parasitized pigs. Many more mast cells were identified after basic lead acetate fixation ('mucosal mast cells', MMC) than after routine formalin fixation ('connective tissue mast cells'). The MMC were preferentially localized in the lamina propria. There were no differences between conventional and gnotobiotic pigs. However, in parasitized animals, the number of mast cells was several times higher, mainly because there were more MMC. The heterogeneity of intestinal mast cells in the pig indicates that this might be an interesting model for functional studies on mast cell subsets.
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PMID:Mast cell heterogeneity in the small intestine of normal, gnotobiotic and parasitized pigs. 247 Jun 84

The mucosal and connective-tissue mast cells (MMC and CTMC, respectively) of the rat are histochemically and functionally distinct. MMC, unlike CTMC, are insensitive to the degranulating action of the mast cell secretagogue Compound 48/80 and instead increase in number after treatment with this drug. T cell-derived growth factors are necessary for the growth of MMC-like cells from hemopoietic tissues in vitro, as well as for nematode-induced MMC proliferation in vivo. We therefore examined the possible role of the thymus in the pharmacologically induced MMC expansion. Mast cell numbers and histamine content after treatment with Compound 48/80 were determined in the skin, tongue and gut of athymic male LEW/MOL-rnu/rnu rats and their normal littermates at the age of 6-7 weeks. The influence of the strain of rat and the mode of administration of the drug was assessed by studying age- and sex-matched Sprague-Dawley rats as well. Injections of Compound 48/80 for 5 days resulted in a statistically significant increase in the number of intestinal MMC and the histamine content of all thymus-bearing rats. The increase was more pronounced in the Sprague-Dawley rats, however, and unrelated to the mode of administration of the drug, indicating that the MMC-stimulating action of Compound 48/80 is at least partly controlled by genetic factors. Athymic rats showed no statistically significant MMC expansion. This suggests that the MMC response after Compound 48/80 treatment may be at least partly dependent on the thymus. The mast cell numbers and histamine content in the tissues of athymic control rats were higher than in their thymus-bearing littermates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thymus dependence of compound 48/80-induced mucosal mast cell proliferation. 349 96

Functional mast cells have been isolated from the lamina propria of the small intestine of rats infected with the nematode Nippostrongylus brasiliensis. The cells released histamine on challenge with specific antigen, anti-rat IgE, concanavalin A, and calcium ionophores but were less responsive than peritoneal mast cells (MMC) from the same animals. Intestinal mucosa mast cells (PMC) were refractory to the action of the basic secretagogues peptide 401 from bee venom and compound 48/80. The anti-allergic compounds disodium cromoglycate (less than or equal to 10(-3) M), AH 9679 (less than or equal to 10(-4) M), and theophylline (less than or equal to 10(-2)) did not inhibit antigen-induced histamine secretion by MMC, although these compounds were effective against PMC. In contrast, doxantrazole (10(-5) to 10(-3) M) inhibited the secretion of histamine from both MMC and PMC in a comparable dose-dependent fashion. Thus, we have established that mast cells from different sites are functionally heterogeneous not only in their response to various stimuli for histamine secretion, but also in their responses to different pharmacologic modulators of secretion. It cannot be assumed that anti-allergic compounds effective against mast cells in one tissue site or organ will be equally efficacious against mast cells in other sites. The extent of this functional heterogeneity must be established, and its investigation may provide new insights into the biochemical events involved in mast cell secretion.
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PMID:Mucosal mast cells. II. Effects of anti-allergic compounds on histamine secretion by isolated intestinal mast cells. 617 39

The behavior of the mast cell population was analyzed during the sequential changes that normal mice skin undergoes during experimental two-stage carcinogenesis. Our study reveals that the number of mast cells increased during the promotion period but that this alteration is confined to the 30-microns-wide strip below the epidermis. A different mast cell phenotype appeared in this area, compatible with an MMC-like phenotype. During the carcinogenesis process, the mast cell population is comprised of two distinct subpopulations that appeared simultaneously in the same tissue, i.e. connective tissue mast cells, normally found in the skin of mice, and the newly formed mucosal mast cell-like cells, currently found in gastrointestinal mucosa.
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PMID:Mast cell phenotypic changes in skin of mice during benzoyl peroxide-induced tumor promotion. 752 Oct 58

Rat peritoneal mast cells and 6-thioguanine-resistant rat basophilic leukemia cells, representative of connective tissue-type (CTMC) and mucosal (MMC) mast cells, respectively, were fused using polyethylene glycol. Four out of 14 primary hybrid mast cell lines contained more than 50% of CTMC as demonstrated by histochemical staining. Two cell lines, one predominantly of the CTMC and the other of the MMC phenotype, were selected for further study. Among these, the phenotype was also confirmed by analysis for rat mast cell protease I and by mediator release triggered by compound 48/80 and ionophore A23187. The CTMC phenotype disappeared after culturing cells for 2 weeks. The change in phenotype did not significantly alter the mediator release due to calcium ionophore A23187. Repeated cloning of cells bearing the CTMC phenotype did not yield a cloned line of cells expressing the CTMC phenotype only, although it prolonged the persistence of this phenotype. During the period of CTMC phenotype loss, a drop in cellular DNA content occurred, suggesting that chromosome instability may, at least partially, have been responsible for the phenotypic changes.
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PMID:Phenotypic changes among hybrid rat mast cells. 758 Feb 87

Activation of MMC-34 cells, a murine mast cell line, or bone marrow-derived mast cells by aggregation of IgE cell surface receptors or addition of calcium ionophore stimulates prostaglandin (PG) D2 synthesis and secretion. An initial rapid burst of PGD2 synthesis, complete within 30 min, is followed by a slower subsequent production of PGD2 that reaches a maximum 4 to 8 h after activation in MMC-34 cells. PG synthase 1 (PGS-1) message and protein are expressed constitutively in MMC-34 cells and are not modulated by exposure to calcium ionophore or aggregation of IgE receptors. In contrast, activation of MMC-34 or bone marrow-derived mast cells induces expression of the PG synthase 2 (PGS-2) gene. PGS-2 induction following mast cell activation is blocked by dexamethasone. The initial PGD2 burst in activated MMC-34 cells is prevented by aspirin pretreatment, suggesting that constitutive PGS-1 present in mast cells before activation is responsible for the early PGD2 production in response to activation. In contrast, the later phase of PGD2 production is blocked by dexamethasone, cycloheximide, or NS-398, a PGS-2-specific nonsteroidal anti-inflammatory drug that inhibits PGS-2 enzyme activity but not PGS-1 activity. These data demonstrate that mast cell activation results 1) in the induction of PGS-2 gene expression, and 2) in both PGS-1-dependent PGD2 synthesis and PGD2 synthesis that is dependent on the activation-induced synthesis and activity of PGS-2.
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PMID:Prostaglandin synthase 1 and prostaglandin synthase 2 both participate in activation-induced prostaglandin D2 production in mast cells. 760 59

The distribution and histochemical characteristics of mast cells in the stroma of cervical squamous cell carcinoma were investigated using different staining methods of alcian blue-safranin, berberine sulphate and toluidine blue. The findings suggest that mast cells in the stroma of the squamous cell carcinoma of the cervix might contain a glycosaminoglycan different from that of typical connective tissue mast cell (CTMC) and mucosal mast cell (MCC). They thus, might be a specific subset of mast cells though sharing some of the staining properties of both CTMC and MMC. In the cervical carcinoma in situ, mast cells were distributed closely around the tumor or the involved glands with great density and the number was significantly higher than that of the invasive carcinoma (P < 0.01). In invasive carcinoma, mast cells were mainly distributed in the deep stroma and the stroma around the tumor, only a few in the stroma within the tumor (P < 0.01). The significance of mast cell reaction in the stroma of squamous cell carcinoma of the cervix is discussed.
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PMID:Distribution and histochemical characteristics of mast cells in stroma of the cervix squamous cell carcinoma. 828 8


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