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)

The proliferative activity of mast cells in the nasal mucosae of allergic (n = 14) and non-allergic (n = 18) rhinopathic patients was studied by a sequential double immunohistochemistry using anti-proliferating cell nuclear antigen (PCNA) and anti-tryptase antibodies. Two hundred to 300 tryptase-positive cells (mast cells) were studied in each allergic nasal epithelium. In case of non-allergic nasal mucosa, only a few mast cells existed in the epithelial layer. The total number of mast cells which we could detect in all patients was 168 cells. One of these cells contained PCNA. Three hundred to 500 mast cells were studied in each subepithelial layer and deep layer of lamina propria of both diseases. PCNA-positive mast cells were observed in the nasal epithelia of 10 allergic patients. In the subepithelial layer, PCNA-positive mast cells were observed eight allergic patients and four non-allergic patients, respectively. In the deep lamina propria, PCNA-positive mast cells were observed in a few patients with both diseases. The percentage of PCNA-positive mast cells of all mast cells each area ranged from 0 to 1.7%. The incidence of PCNA-positive mast cells was statistically higher in the allergic epithelium and subepithelial layer than in the deep layer of lamina propria. Moreover, that of PCNA-positive mast cells in the subepithelial layer was higher in allergic than in non-allergic nasal mucosa. Our results suggest that mast cell proliferation may contribute to the number of mast cells in the nasal epithelium and subepithelial layer of allergic patients.
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PMID:Proliferative activity of mast cells in allergic nasal mucosa. 775 10

In this study, age, sex, recurrence, metastasis, death rate, and histologic patterns were in agreement with those of previous reports on canine mast cell tumors. Histologic grading, mitotic index, chromosome nucleolar organizer regions stained with silver (AgNORs), and anti-proliferating cell nuclear antigen (PCNA) were evaluated as indicators of prognosis. Histologic grading, AgNORs estimated in 100 cells, and PCNA-labeled fraction estimated in five high power fields (HPFs) were significantly different between recurring and nonrecurring tumors. Those prognostic factors were also significantly different between tumors that metastasized and those that did not. The survival time was lower in dogs with mast cell tumors with histologic grade 3 (Patnaik's), AgNOR counts higher than 2.25, and PCNA count in five HPFs higher than 261. The significance of these factors as markers for prognosis determined by logistic regression analysis differed with the time period considered. By combining the three most significant prognostic factors in a prognostic index, three models were obtained to determine the probability of nonrecurrence at 3, 6, and 9 months after surgery. The models were accurate in the prediction of the outcome of up to 80% of mast cell tumors. The use of these models provides a less subjective means of prognosticating mast cell tumors than the use of any one component alone.
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PMID:Prognosis of canine mast cell tumors: a comparison of three methods. 786 78

The expression of PCNA and EGFr in chemically induced hepatocellular carcinoma of liver and squamous cell carcinoma of stomach in rats were immunohistochemically observed. The results showed that the carcinoma cells of both tumors revealed a positive immunreaction to PCNA and EGFr. The histochemical observation of mast cell (MC) in both tumor tissues showed that the amount of MC in the surroundings of tumor cell nests was markedly different. According to the amount of the surrounding MCs the tumor cell nests could be divided into two groups: Group A with abundant MC infiltration and Group B with only scarce or without MC infiltration. The PCNA-positive cells in the tumor cell nests of both groups were calculated respectively. The results revealed that the amount of PCNA-positive cells in the group B was markedly more than that in the group A. The numerical ratio between two groups was 3:1 in the liver carcinoma and 2:1 in the stomach carcinoma approximately. An overexpression of EGFr was observed in tumor tissues of both groups, but there was also a marked difference in the amount of positively expressed cells and in the intensity of their staining reaction between both groups. The positively expressed cells in group B were much more and their staining intensity was much stronger than those in group A. According to the above mentioned results of observation, the expression state of both factors (PCNA and EGFr) was basically identical, suggesting that the MC may possess some inhibitory effect upon the growth rate of tumor cells of the experimental hepatocellular carcinoma of liver and the squamous cell carcinoma of stomach in rats.
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PMID:The relationship between mast cell infiltration and the expression of PCNA and EGFr in experimental hepatocellular carcinoma of liver and squamous cell carcinoma of stomach in rats. 875 35

The time-course of differentiation/proliferation of mast cells in gut epithelium was investigated in mice infected with the nematode Strongyloides venezuelensis. After infection, expression of proliferating cell nuclear antigen increased in gut intraepithelial mast cells on days 7 to 11, followed by an increase in the number of intraepithelial mast cells from days 11 to 14. Mast cell precursors were defined as cells that formed mast cell colonies in methylcellulose culture. After infection, the numbers of mast cell precursors in the population of gut intraepithelial mononuclear cells (IEMNC) increased significantly on day 3 and returned to the pre-infection level by day 7. Mast cell precursors in Peyer's patches, mesenteric lymph nodes (MLN), and spleen also increased from day 7 p.i. Production of IL-3 and IL-4 in MLN and spleen were increased between 7 and 11 days p.i. These results show that murine intestinal mastocytosis is initiated by an early increase in mast cell precursor number in the gut epithelium followed by proliferation/differentiation of mast cells. Mast cell precursor numbers increased even before the production of IL-3 and IL-4 in MLN and spleen, suggesting that some local factors might be involved in this phenomenon.
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PMID:Early increase of gut intraepithelial mast cell precursors following Strongyloides venezuelensis infection in mice. 905 24

The role of mast cells and their main secretory products in the effects of oestradiol on the uterus was investigated. Ovariectomized rats were treated with a single injection of oestradiol (10 micrograms per rat, i.m.) or vehicle together with drugs affecting the activity of mast cells, cromoglycate (10 mg per rat, i.m.), which diminishes the degranulation of mast cells, or compound 48/80 (0.5 mg per rat, i.m.), which enhances this process. Oestradiol or vehicle was also administered with two important secretory products of mast cells, heparin (0.4 mg per rat, i.m.) or histamine (2 mg per rat, i.m.). All drugs were injected simultaneously with oestradiol (first injection) and then every 6 h until the animals were killed. Observations were performed at 24, 36 and 48 h after oestradiol or vehicle injection. The condition of mast cells was determined by the percentage of degranulated mast cells in sections stained with toluidine blue. Oestradiol-induced effects in the uterus were estimated by the mitotic index, proliferating cell nuclear antigen-labelling index, DNA content, volumes of cells, nuclei and nucleoli in the luminal epithelium, glandular epithelium and stroma cells of the endometrium. Cromoglycate treatment resulted in a decrease in both mast cell degranulation and all examined oestradiol effects in the uterus at all periods of observation. Compound 48/80 increased mast cell degranulation and expression of one aspect of oestradiol effects on the volumes of cell compartments. Histamine or heparin led to a marked increase in the cell, nucleus and nucleolus volumes in all uterine structures. However, heparin produced a depression in proliferation, whereas histamine had a weak transient stimulating action on this process. No effects of the protocols were found in the absence of oestradiol treatment. These results suggest that mast cells are involved in the realization of oestrogen action, including the stimulation of cell growth and proliferation in the uterus, and that the effect of mast cells is mediated by both histamine and heparin.
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PMID:Role of mast cells in oestradiol effects on the uterus of ovariectomized rats. 971 77

We studied the effects of stem cell factor (SCF) on human skin mast cell (HSMC) survival and the proliferation of neurofibroma (NF) cells in transplanted NF in nude mice. Small pieces of cutaneous NF from a patient with von Recklinghausen's disease were transplanted subcutaneously into nude mice. Recombinant human SCF (10 or 100 ng) was injected six or seven times around the NF transplantation sites over 11 days (i.e. every other day). The number of HSMCs was reduced in vehicle-injected NF compared to the amount present before transplantation. In contrast, NF-transplanted animals that were injected with SCF (10 or 100 ng) showed preservation of mast cell numbers in the tissue. Using computerized image analysis, mast cell size in SCF-treated NF transplants was significantly altered (larger at the 10 ng dose, and smaller at the 100 ng dose) compared with the size before transplantation or in vehicle-injected tissue. Furthermore, at the higher SCF dose (100 ng) PCNA-positive NF cells showed a significant increase. These results indicate that HSMCs in transplanted NF tissue retain their capacity to respond to SCF in vivo, and that SCF contributes to the regulation of both HSMC survival and size in cutaneous NF. In addition, activated HSMCs induced by SCF may be involved in the growth of cutaneous NF in von Recklinghausen's disease. Thus, this experimental model may be useful in the study of the cellular interactions between HSMCs and other stromal cells in cutaneous NF.
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PMID:Local injection of recombinant human stem cell factor promotes human skin mast cell survival and neurofibroma cell proliferation in the transplanted neurofibroma in nude mice. 1042 Oct 57

Stable transduction of genetic material, in combination with sensitive methodologies for in vivo study of cell physiology, provides an opportunity to efficiently evaluate the functions of regulatory proteins. To dissect the minimal therapeutic function of such proteins, we have stably expressed protein microdomains as fusions, composed of short peptides, and detected specific subfunctions distinct from holoprotein function, using flow cytometry and other techniques. We demonstrate that retroviral delivery of the 24-amino-acid proliferating cell nuclear antigen-binding motif (p21C), derived from the C-terminus of the cell cycle inhibitor protein, p21, is sufficient to induce cell cycle arrest. Cells expressing this peptide motif reversibly execute both G1- and G2-checkpoint controls that are normally activated subsequent to interference with DNA synthesis. The p21C effect is distinct from results obtained with an intact p21 protein that also binds cyclin-CDK complexes and arrested cells exclusively at the G1/S transition. Thus, microdomains can exert unique biological effects compared to the parental molecules from which they were derived. To further evaluate the peptide delivery strategy, we analyzed the role of various kinases in IgE-mediated stimulation of mast cell exocytosis. Primary bone marrow-derived mast cells were transduced with retroviral constructs encoding short-kinase inhibitor motifs and analyzed by flow cytometry for effects on exocytosis. We found that a specific protein kinase A (PKA) inhibitor peptide suppressed IgE-mediated stimulation of mast cell exocytosis. This anti-exocytotic effect was mimicked by a small molecule inhibitor of PKA (KT5720). Thus, the ability to express protein microdomains can be a powerful means to subtly perturb cellular physiology in manners that reveal new paths for therapeutic intervention. We believe that such approaches might allow for new forms of gene therapy to become available.
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PMID:Retroviral delivery of peptide modulators of cellular functions. 1093 65

We determined the distribution of mast cells in nasal mucosa and studied their proliferation. Inferior turbinate mucosa was sampled in 13 patients with allergic rhinitis (allergic group) and 5 without (non allergic group) and stained immunohistochemically using anti mast cell tryptase antibody, anti-c-kit antibody, anti-PCNA antibody, and anti mast cell chymase antibody. Tissue sections stained with anti tryptase antibody revealed a higher degree of infiltration of tryptase-positive cells, i.e., mast cells, in the allergic group than in non allergic group. In the allergic group, the number of tryptase-positive cells, c-kit-positive cells, and PCNA-positive cells was significantly greater in the epithelium and shallow lamina propria than that in the deep lamina propria. Tryptase-positive, c-kit-positive cells, i.e., c-kit-positive mast cells, and tryptase-positive, PCNA-positive cells, i.e., PCNA-positive mast cells, were also abundunt in the epithelium and shallow lamina propria. The stem cell factor and c-kit receptor are reported to play a primary role in mast cell differentiation and proliferation. PCNA-positive cells represent actively proliferating cells. Based on the above, we concluded that mast cells in the epithelium and shallow lamina propria in the allergic group differentiated and proliferated more actively than those in the deep lamina propria.
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PMID:[Differentiation and proliferation of mast cells in nasal mucosa]. 1143 40

We previously reported mast cell increases in H. pylori gastritis. To determine the mechanism, we investigated the kinetics of mast cells and mast cell growth factor (stem cell factor, SCF) in H. pylori-positive and -negative gastric mucosa. Biopsy specimens from 12 H. pylori-negative and 28 positive subjects were examined. Sections were stained for mast cells, proliferating cell nuclear antigen (PCNA), and SCF. Densities of mast cells, PCNA-positive mast cells, and SCF-positive cells were significantly greater in H. pylori-positive than -negative subjects. SCF was expressed in mast cells and fibroblasts. The density of SCF-positive fibroblasts increased in H. pylori-positive gastritis and decreased after cure of infection. SCF mRNA was detected in H. pylori-positive gastric mucosa. Fibroblasts isolated from the normal gastric mucosa expressed SCF mRNA after incubation with H. pylori water extract. SCF may be one of the factors for mast cell increase. Fibroblasts may participate in mast cell increase and inflammation in H. pylori infection.
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PMID:Stem cell factor expressed in human gastric mucosa in relation to mast cell increase in Helicobacter pylori-infected gastritis. 1185 41

Dorsal skin responses to a subchronic UVB-irradiation (10kJ/m2/rat /day), were examined in Wistar-derived hypotrichotic WBN/ILA-Ht rats for up to 3 months. Hyperplasia of epidermal cells and hair follicle epithelial cells as well as parakeratosis developed at 1 month and progressed thereafter, resulting in a prominent epidermis thickening and formation of epidermal ingrowths projecting into the dermis. At the same time, the percentage of proliferating cell nuclear antigen (PCNA)-positive epidermal cells significantly increased after I month. In some portions of the hyperplastic epidermis, especially of the epidermal ingrowths, keratinocytes were somewhat pleomorphic and migrated into the dermis. In the upper dermis, edema with capillary congestion, mast cell infiltration and fibroblast proliferation developed at I month, and the intensity of edema and the number of dermal mast cells was most prominent at 3 months. Edema spread to the epidermis, resulting in intercellular edema and subsequent dissociation of epidermal cells. Degeneration of collagen fibers was also detected in the upper dermis, especially beneath the epidermis. In addition, although not significant because of a large individual difference, the serum IgE concentration, showed a tendency to increase after 2 months. The present study clarified the characteristics of the dorsal skin responses to a subchronic UVB-irradiation in rats.
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PMID:Dorsal skin responses to subchronic ultraviolet B (UVB)-irradiation in Wistar-derived hypotrichotic WBN/ILA-Ht rats. 1216 75


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