Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present investigation was undertaken to determine whether or not there are histochemical and morphological changes in the intestine of the chronically reserpine-treated rat, an animal model of cystic fibrosis. Male Sprague-Dawley rats were given seven daily intraperitoneal injections of reserpine at dosages of 0.5 (n = 6) or 1.0 mg/kg body weight (n = 6). Control groups consisted of parfed solvent-injected (n = 6), solvent-injected (n = 4), and saline-injected animals (n = 4). Light microscopic histochemical procedures and morphological assessments were performed on sections of "Swiss rolls" of small and large intestine. Chronic reserpine treatment caused an increase in the sulfation of goblet cell mucin in the small intestine without accompanying morphological change; these findings resemble those reported in cystic fibrosis. No qualitative differences in mucin were found in the large intestine but there was an increased number of goblet cells in the surface epithelium and retention of mucus within these cells. Similar although less marked changes were noted in the parfed controls suggesting that those observed in the treated groups may be due, in part, to the reserpine-induced anorexia. The resemblance between the changes in the small intestine of the reserpine-treated rat and those observed in CF patients supports the contention that the chronically reserpine-treated rat is suitable as a model of cystic fibrosis.
Exp Mol Pathol 1987 Aug
PMID:Morphological and histochemical changes in intestinal mucosa in the reserpine-treated rat model of cystic fibrosis. 360 43

Supernatants of cultures and extracts of Trypanosoma rangeli readily release N-acetyl neuraminic acid from a variety of substrates. The activity in both supernatant and cell extract is precipitated between 30 and 50% ethanol, and between 40 and 70% ammonium sulfate. Fractionation of the culture supernatant by gel exclusion gives a single peak of neuraminidase activity of molecular weight 48 000. The culture supernatant releases sialic acid at different rates from the following substrates:fetuin, sialyllactose and orosomucoid but not from bovine submaxillary mucin and ovomucoid. The enzyme in the culture supernatant is also active against human erythrocytes of all ABO types. The enzyme showed an optimum pH of 5.0 for sialyllactose and erythrocyte substrates. Large amounts of the enzyme are preferentially secreted during growth in vitro.
Mol Biochem Parasitol 1985 Apr
PMID:Neuraminidase activity in Trypanosoma rangeli. 399 Jul 12

Monoclonal antibody (McAb) F36/22, raised against a human breast tumor line, identifies an antigen found in the circulation of cancer patients. Antigen was purified from malignant effusions using McAb-affinity chromatography followed by adsorption-desorption from immobilized wheat germ lectin. Electrophoretic analysis demonstrated the isolation of a single high mol. wt glycoprotein exhibiting an isoionic point near pH 4.2 and a density of approx. 1.45 g/ml. Although highly reactive with wheat germ lectin, a negligible or weak interaction was observed with concanavalin A, lentil and peanut agglutinin. The antigen was immune-precipitable, indicating the occurrence of multiple McAb-binding sites, and was resistant to heat and acid treatments. Antigenicity was not perturbed following protease or neuraminidase treatments, but was affected upon exposure to alkaline conditions. Taken together, these data suggest that McAb F36/22 recognizes a high mol. wt component occurring in circulation as a mucin-like glycoprotein.
Mol Immunol 1984 Oct
PMID:Immunoaffinity isolation of ductal carcinoma antigen using monoclonal antibody F36/22. 609 73

A mucosal defect was produced by cryosurgery in the antral and the fundic wall of the rat stomach, and regeneration of gastric endocrine cells was studied 50, 100 and 200 days after operation. Fifty days after the operation, the mucosal defect was completely covered with regenerated epithelium. The regenerated mucosa both in the antral and in the fundic region consisted of mucinous glandular structures. The regenerated mucosa in the corpus remained pseudopyloric in type even 200 days after operation. Regardless of the time after operation, regeneration of endocrine cells was always observed. We could identify G cells and EC cells in the regenerated mucosa of the antrum, and EC cells, A cells and AL cells in the regenerated mucosa of the corpus, respectively. By electron microscopy, endocrine-exocrine cells were frequently encountered. These cells had two different types of intra-cytoplasmic granules; one was an endocrine-specific, small electron-dense granule, and the other a large, lucent mucin droplet-like granule. These findings indicate that the endocrine cells of the stomach are formed from endodermal precursor cells.
Virchows Arch B Cell Pathol Incl Mol Pathol 1982
PMID:Regeneration of endocrine cells in the stomach. 612 10

The histochemical staining, labeling index and incorporation of [3H] thymidine [TdR] in large intestinal epithelium were compared in four anatomically distinct segments from ICR/Ha and C57Bl/Ha mice. This comparison was done because the incidence of 1,2-dimethylhydrazine (DMH)-induced carcinomas is different for different anatomic segments as well as for the two strains. Within each strain, the amount of [3H] TdR incorporated into mucosal DNA was found to vary less than 20% at each anatomic site of the large intestine. However, there were site-specific differences in the depth of the proliferative populations within the crypts. In autoradiograms from both strains, the crypts of the proximal colon showed maximal [3H] TdR labeling of nuclei in mid-crypt cells, some of which contained mucin. In contrast, the distal colon and rectum were characterized by maximal nuclear labeling in a population of undifferentiated cells near the base of each crypt. In distal ICR/Ha colon, the proportion of labeled nuclei at each crypt depth corresponded to the [3H] TdR labeling of DNA that had been isolated from frozen sections cut sequentially. As visualized with alcian blue-periodic acid Schiff (AB-PAS) and high iron diamine-alcian blue (HID-AB) stains, the epithelial mucin showed site-specific differences, but the differences between the two strains of mice were not remarkable. In contrast to the human and rat large intestine, the acidic mucin in the mouse large intestine was predominantly sialomucin. However in the cecum and mid-distal colon, there was a predominance of sulfomucin. In the various anatomic segments of both strains, the histochemical staining, labeling index and incorporation of [3H]TdR were remarkably similar considering the large differences in susceptibility to chemically-induced neoplastic change.
Virchows Arch B Cell Pathol Incl Mol Pathol 1982
PMID:A comparative study of the normal histochemical and proliferative properties of the large intestine in ICR/Ha and C57Bl/Ha mice. 613 79

We have studied the ultrastructure of glycocalyx at the luminal surface of normal and diseased urothelium from humans and rats with ruthenium red staining. A correlation between the thickness and staining intensity of the glycocalyx and the surface topography of the luminal surface was observed. An intensely stained thick glycocalyx was associated with prominent surface microvilli seen in the following conditions in humans: some control urothelium, inverted papilloma, well and moderately differentiated transitional cell carcinomas and mucin producing adenocarcinomas. These changes were also present in rats with FANFT-induced preneoplastic and neoplastic changes. A thin glycocalyx was associated with a scalloped luminal surface containing asymmetric unit membrane plaques and was found in some control humans urothelium and in normal rat urothelium. A thin glycocalyx was also associated with the relatively smooth surface seen in poorly differentiated transitional cell carcinomas as well as in some mucin producing adenocarcinomas. We suggest that urothelial glycocalyx, as demonstrated by ruthenium red staining, correlates with the luminal surface topography rather than specific pathological conditions of the bladder.
Virchows Arch B Cell Pathol Incl Mol Pathol 1983
PMID:Cell surface coat of human and rat bladder urothelium. I. Ruthenium-red studies in non-neoplastic and neoplastic cells. 619 Mar 6

A gastric mucosal mucin receptor has been isolated from the epithelial cell membrane by affinity chromatography on wheat germ agglutinin. The receptor protein displayed an apparent molecular weight of 97kDa and exhibited binding specific to gastric mucin in a concentration-dependent manner. The binding of mucin to the mucosal receptor was inhibited by lipopolysaccharide from H. pylori. The inhibitory effect was proportional to the concentration of lipopolysaccharide up to 30 micrograms/ml, at which concentration a 91% decrease in binding occurred. The results suggest that H. pylori lipopolysaccharide is capable of disrupting the integrity of mucus perimeter of gastric mucosal defense by interfering with epithelial cell-mucin binding.
Biochem Mol Biol Int 1993 Dec
PMID:Inhibition of gastric mucosal mucin receptor by Helicobacter pylori lipopolysaccharide. 751 19

The mucin isolated from gastric secretion of duodenal ulcer patients before and after therapy with a new antiulcer agent, ebrotidine, was assessed for H. pylori aggregating activity and macromolecular organization. Analyses of mucin molecular forms revealed that successful therapy with ebrotidine was accompanied by a 2.6-2.9-fold increase in the high molecular weight mucin form. The H. pylori aggregation inhibition assays showed that therapy with ebrotidine evoked a 4-fold increase in mucin anti-H. pylori titer. The changes in the functional properties of mucin following ebrotidine therapy were also accompanied by a 36% increase in the content of sulfomucin. The results demonstrate that ulcer therapy with ebrotidine lead to a marked enhancement in mucin's qualities associated with maintenance of gastric mucosal integrity and strengthening the indigenous defenses against H. pylori.
Biochem Mol Biol Int 1994 Nov
PMID:Helicobacter pylori aggregating activity of gastric mucin with ulcer healing by ebrotidine. 753 17

The purpose of this study was to determine the biochemical and molecular characteristics of mucin synthesized by cystic fibrosis cells (CFPAC-1), a pancreatic cancer cell line derived from a patient with cystic fibrosis, and pancreatic cancer (SW-1990) cell lines. High molecular weight glycoproteins (HMG) were quantified by [3H]-glucosamine labeling and chromatography on sepharose CL-4B. Mucin gene expression was determined by using cDNA probes for 2 distinct intestinal mucins (MUC2 and MUC3) and one stomach mucin (MUC1). The specific mucin core epitopes were confirmed by immunoblots using antibodies that recognize T, Tn, sialosyl Tn, MUC1, MUC2, and MUC3. The results of these experiments demonstrate that CFPAC-1 cells contained 1.25 fold and 1.4 fold more HMG in the membrane and cytosolic fractions, however, secreted 4-fold more HMG into the medium compared to SW-1990 cells. The HMG of SW-1990 was found to be mucinous in nature and not proteoglycans, as it was not susceptible to hyalurinidase, heparinase and chondroitinase ABC. The HMG of CFPAC-1 was also predominantly (80%) mucinous but with small amounts of proteoglycans. mRNA and immunoblot analysis suggest that these CFPAC-1 and SW-1990 cells predominantly express MUC1 apomucin, small amounts of MUC2 apomucin, and no MUC3. Pulse chase labeling and immunoprecipitation of MUC1 type mucin using the 139H2 monoclonal antibody demonstrated that different sizes of mucin gene product were present in both cell lines, corresponding to the known length polymorphism of this mucin. Both T and Tn antigens were significantly higher in CFPAC-1 and SW-1990 cells as compared to sialosyl Tn antigen. These findings were associated with the increased activities of polypeptidyl N-acetylgalactosaminyl transferase and b1,3-galactosyltransferase. These investigations demonstrate for the first time that cystic fibrosis cells (CFPAC-1) secrete and synthesize high amounts of mucin which is associated with high levels of MUC1 mRNA, low levels of MUC2 mRNA and non detectable MUC3 mRNA.
Biochem Mol Biol Int 1995 Feb
PMID:Cystic fibrosis and pancreatic cancer cells synthesize and secrete MUC1 type mucin gene product. 754 50

Primary cultures of guinea pig tracheal epithelial cells in air/liquid interface were exposed to one of four agents associated with airway inflammation: the peptide histamine (100 microM), the lipid mediator platelet-activating factor (1 microM), the cytokine tumor necrosis factor-alpha (15 ng/ml; specific activity 2.86 x 10(7) U/mg), or enzymatically generated reactive oxygen species (purine [500 microM]+xanthine oxidase [20 mU/ml]). Effects of each of these substances on release of mucin by guinea pig tracheal epithelial (GPTE) cells were measured using a monoclonal antibody-based enzyme-linked immunosorbent assay (ELISA). Each secretagogue significantly enhanced release of mucin, but the stimulatory effect of each was inhibited by pre-(+)co-incubation of the cells with the competitive inhibitor of nitric oxide synthase, NG-monomethyl-L-arginine (L-NMA), but not by NG-monomethyl-D-arginine (D-NMA), the inactive stereoisomer that does not inhibit nitric oxide synthase. Neither L-NMA nor D-NMA affected mucin secretion by themselves. The results suggest that each of these inflammation-associated mediators provokes airway epithelial mucin secretion via a mechanism involving intracellular production of nitric oxide (NO) as a critical signaling molecule.
Am J Respir Cell Mol Biol 1995 Nov
PMID:Hypersecretion of mucin in response to inflammatory mediators by guinea pig tracheal epithelial cells in vitro is blocked by inhibition of nitric oxide synthase. 757 87


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