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)

Intestinal mucosal mast cells (IMMCs) are closely apposed to nerves, which is consistent with other evidence suggesting that mast cells are innervated. Recent studies have indicated that coordinated changes in mast cell and nerve densities occur in the gut mucosa, during progressive fibrosis, but there is a lack of experimental evidence to support remodeling of intestinal nerve fibers as part of a disease process. Infection of rats with the nematode Nippostrongylus brasiliensis (Nb) results in an initial loss of stainable IMMCs, during an acute inflammatory phase, with subsequent mast cell hyperplasia. Accordingly, we employed the Nb model to look for structural neuroplasticity of intestinal mucosal nerves during inflammation. Immunocytochemical labeling of neurofilament subunits was very low in the jejunal mucosa of all animals, whereas neuron-specific enolase (NSE)-immunoreactive nerves were relatively abundant in control animals. The number of NSE-immunoreactive profiles increased approximately 2.5-fold by day 10 (d10) postinfection (p less than 0.01) and returned to near control values by d14. Immunoreactivity for B-50/GAP-43 was more extensive, labeling more than four times the number of nerves per villus, compared with NSE (p less than 0.0001). B-50 immunoreactivity decreased minimally (ca. 20%) by d7 postinfection, and then increased through control values between d10 and d21, to 30% greater than controls at d49 (p less than 0.05). Subclassification of the B-50-immunoreactive nerves according to cross-sectional area revealed a greater than twofold increase in the proportions of large fibers at d7 and d10. Subsequently, the proportions of small nerves were increased compared with controls. The fiber size changes were found to correlate with mast cell densities (r = -0.72 for large and r = 0.76 for small nerves). At d10, dilated B-50- and NSE-immunoreactive nerves predominated, and extraneuronal NSE was noted. Electron microscopy revealed that this was due to axonal dilation and degeneration. These data provide evidence for plasticity of intestinal mucosal nerve fibers during inflammation. This includes early degenerative and later regenerative phases that appear to correlate with mast cell densities. The phenotype of mucosal nerves in control animals suggests ongoing modeling of these fibers.
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PMID:Remodeling of B-50 (GAP-43)- and NSE-immunoreactive mucosal nerves in the intestines of rats infected with Nippostrongylus brasiliensis. 183 18

Inflammatory or allergic conditions, as well as situations where healing and repair processes occur, are characterized by the presence of increased numbers of mast cells. Previous work on the effect of neuropeptides on mast cell mediator release showed that only substance P caused such release from intestinal mucosal mast cells [Shanahan, F., Denburg, J. A., Fox, J., Bienenstock, J. & Befus, A. D. (1985) J. Immunol. 135, 1331-1337]. Accordingly, we investigated the microanatomical relationship between mast cells and enteric nerves in normal rat intestine and parasite-infected rat intestine, in which mucosal mast cell hyperplasia occurs. Combined immunohistochemistry for neuron-specific enolase and staining with alcian blue at pH 0.5 was employed on paraffin-embedded sections of normal and Nippostrongylus brasiliensis-infected rat jejunum. Sixty-seven percent of intestinal mucosal mast cells were touching subepithelial nerves, and an additional 20% were within 2 micron of nerves. Assessment of the proportion of the lamina propria occupied by mast cells (12.5%), the average mast cell area (121 +/- 28 microns 2), and the density of enteric nerves (one per 788 +/- 151 microns 2) suggested that the association was 5 times greater than would be expected by chance alone (P less than 0.0001). In consecutive sections, the nerves in contact with mast cells were also shown to contain substance P and/or calcitonin-gene-related peptide. Electron microscopy confirmed this association: 8% of the mast cells in infected rats exhibited membrane-membrane contact with unmyelinated axons containing 70- to 170-nm dense-core vesicles, and an additional 31% were situated less than 250 nm from nerves. Other mast cells appeared to embrace nerve bundles through the projection of lamellopodia. These data provide systematic quantitative evidence that a structural foundation for communication between the immune and nervous systems exists in the rat gastrointestinal tract.
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PMID:Intestinal mucosal mast cells in normal and nematode-infected rat intestines are in intimate contact with peptidergic nerves. 243 89

Sixty-five canine skin neoplasms studied using immunocytochemistry, included 22 histiocytomas, 18 amelanotic melanomas, 14 cutaneous lymphosarcomas, six mast cell tumors, and five transmissible venereal tumors. Formalin-fixed, paraffin-embedded sections were stained using the avidin-biotin-peroxidase complex (ABC) immunoperoxidase technique for reactivity with S-100 protein, kappa and lambda immunoglobulin light chains, alpha-1-antitrypsin, alpha-1-antichymotrypsin, leukocyte common antigen (LCA), neuron-specific enolase, keratin, cytokeratin, muramidase, and vimentin. Detection of S-100, kappa and lambda light chains, neuron-specific enolase, and vimentin were most useful for screening these neoplasms. None of the markers examined was consistent in staining histiocytomas. While reactivity of S-100 (ten cases) and neuron-specific enolase (ten cases) was detected in some amelanotic melanomas, lambda light chain immunoglobulin (eight cases) was relatively consistent in cutaneous lymphomas. Mast cell neoplasms reacted with avidin and, therefore, were positive, even on negative control sections. Vimentin reacted strongly on all amelanotic melanomas and transmissible venereal tumors examined. These antibodies are helpful adjuncts in the differential diagnosis of canine skin tumors.
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PMID:Diagnostic immunohistochemistry of canine round cell tumors. 313 15

The original form of beta beta enolase (EC 4.2.1.11) in tissue is modified to two more electrophoretically distinct forms when incubated with human serum. The three postsynthetic forms are designated beta beta 3, beta beta 2, and beta beta 1, in order of increasing anodal mobility and increasing modification. Serum and carboxypeptidases A and B all produce identical modifications of beta beta enolase but exhibit very different pH-activity profiles. A purified human serum protein previously named "modifying protein," which is responsible for the modification of creatine kinase-M and alpha-enolase subunits, modifies beta beta enolase and also has a pH-activity profile identical to that for serum. Thus we conclude that the modifying protein is not identical to either carboxypeptidase A or B; it may, however, be an as-yet-undescribed carboxypeptidase. With increased modification, both alpha alpha and beta beta enolase decrease in apparent activation energy; gamma gamma enolase shows no evidence of modification, and its apparent activation energy remains stable. Measurement of activation energy is an easy tool for screening for postsynthetic modifications in an enzyme.
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PMID:Postsynthetic modification of human enolase isoenzymes. 359 9

We report the morphological characteristics of 30 cases of sclerosing hemangioma (SH) of the lung and explore the histological origin of the major cells in these tumors. In addition to routine light and electron microscopy, immunohistochemistry was performed by using 12 monoclonal primary and 5 polyclonal primary antibodies. These included surfactant protein B (SP-B), thyroid transcription factor-1 (TTF-1), mast cell trypsin, CD68, epithelial antigen markers (high molecular weight cytokeratin, low molecular weight cytokeratin [CK-L], epithelial membrane antigen [EMA], cancer embryonic antigen), mesothelial antigen, neuroendocrine markers (neuron-specific enolase [NSE], chromogranin A, synaptophysin, calcitonin, adrenocorticotropic hormone, human growth hormone [hHG]), vimentin, and CD34. Surface cuboidal cells have short microvilli and have lamellar bodies in their cytoplasm. They can sometimes merge into multinuclear giant cells. Immunohistochemical results showed that these cells are strongly positive for SP-B, TTF-1, CK-L, EMA, and cancer embryonic antigen, whereas polygonal cells, previously also described as round or pale cells, were strongly positive for vimentin and TTF-1, and positive or weakly positive for 2 to 3 kinds of neuroendocrine markers. Sparse neuroendocrine granules and abundant microfilaments were observed in their cytoplasm. Some cell clusters in the solid regions were positive for SP-B and EMA. Mast cells existed sparsely in almost every field. Both cuboidal and polygonal cells were negative to CD34 and mesothelial antigen staining. We conclude that cuboidal cells of SH originate from reactive proliferating type II pneumocytes, which can fuse into multinuclear giant cells. Polygonal cells, as true tumor cells, likely originate from multipotential primitive respiratory epithelium and possess the capability for multipotential differentiation. The antibodies of SP-B, TTF-1, vimentin, and CK-L are very helpful to diagnosis and differential diagnosis of SH.
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PMID:Immunohistochemical and ultrastructural markers suggest different origins for cuboidal and polygonal cells in pulmonary sclerosing hemangioma. 1511 33