Disease relevance of LOC442975

• Gelation of mucin precedes the precipitation of cholesterol liquid and solid crystals and the development of gallstones [1].
• These findings suggest that prostaglandins do not regulate gallbladder mucin secretion in the prairie dog, and it is unlikely that increases in gallbladder prostaglandin synthesis are responsible for mediating gallbladder mucin hypersecretion during cholelithiasis in the prairie dog [2].
• To further establish the relationship between mucin and phospholipid secretion, two gastric cancer cell lines, Hs746T and KATO III, were studied [3].
• LPS, derived from Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa (200 microg/mL), all caused an increase in mucin secretion by the DGBE cells, without causing concomitant cell lysis [4].
• Effect of cyclosporine on conjunctival mucin in a canine keratoconjunctivitis sicca model [5].

High impact information on LOC442975

• This suggests that gallbladder mucin is a nucleation matrix for cholesterol gallstones [1].
• Consistent with this, lavage fluid from the airways of allergen-challenged dogs stimulated mucin synthesis severalfold more potently than that from non-allergen-challenged dogs [6].
• Model bile and bile salts accelerate mucin secretion by cultured dog gallbladder epithelial cells [7].
• At a concentration of 0.5 mmol/L, only the more hydrophobic bile salts taurochenodeoxycholate and taurodeoxycholate, but not the hydrophylic bile salts taurocholate and tauroursodeoxycholate, stimulated mucin secretion (P < 0.01) [7].
• PGE2 has no direct role in the synthesis of canine gastric mucin but stimulates release of surface-active phospholipids [8].

Chemical compound and disease context of LOC442975

• Lipopolysaccharide from Escherichia coli stimulates mucin secretion by cultured dog gallbladder epithelial cells [4].
• A method of quantitation of mucin using chondroitin sulfate A as a standard has been modified and applied to timed mucin collections from surgically created isolated colonic fistulas in 8 dogs [9].

Biological context of LOC442975

• Methylation analysis of product formed either with mucin acceptor or Gal beta 1-3GalNAc-alpha-O-benzyl indicated GlcNAc transfer to either carbon 4 or carbon 6 of the GalNAc residue of the acceptors [10].
• Alignment of the amino acid sequences inferred from the cDNA nucleotide sequences showed that BS-C-1 and CV-1 havcr-1 differed from GL37 havcr-1 by having two substitutions in the Cys-rich region, N48H and K108Q, and 10 to 11 additional substitutions plus the insertion of 18 to 22 amino acids in the mucin-like region [11].
• We investigated how different patterns of [Ca(2+)](i) signals evoke salt secretion via ion transport mechanisms and mucin secretion via exocytosis in dog pancreatic duct epithelial cells (PDEC) [12].
• However, no effect of the presumed altered membrane fluidity on TUDC (10 mM)-induced mucin secretion was observed [13].
• In the present study we have investigated whether established second messenger pathways are involved in bile salt-induced mucin secretion [14].

Anatomical context of LOC442975

• The synthesis and release of mucin and phospholipid are functions of the mucous cell that play a critical role in the primary defense of gastric epithelium [3].
• Using immunocytochemical and biochemical techniques, mucin synthesis and secretion were confirmed by these cell lines [3].
• During absorption, NNK was distributed within the entire depth of the mucosa to the tracheal cartilage; however, a portion was conspicuously bound to the mucin component of the mucous lining layer [15].
• Mucin synthesis. II. Substrate specificity and product identification studies on canine submaxillary gland UDP-GlcNAc:Gal beta 1-3GalNAc(GlcNAc leads to GalNAc) beta 6-N-acetylglucosaminyltransferase [16].
• This protein, gp40, was characterized as an O-glycosylated (mucin-type) integral membrane protein of 40 kDa, which was predominantly localized on the apical plasma membrane of filter-grown cells [17].

Associations of LOC442975 with chemical compounds

• Aspirin given to prairie dogs inhibited mucin hypersecretion and gel accumulation and prevented gallstone formation without influencing the cholesterol content of supersaturated bile [1].
• Purified mucin in the concentration of 0.5-2 mg/mL of glycoprotein led to a significant dose-dependent increase in phospholipid solubility, suggesting the formation of a glycoprotein-phospholipid complex [3].
• Furthermore, incubation of explants with 10(-5) mol/L indomethacin failed to prevent in vitro mucin hypersecretion in cholesterol-fed animals [2].
• Some studies have suggested that gallbladder mucin hypersecretion is mediated by increases in gallbladder prostaglandin synthesis, but other observations are difficult to reconcile with this view [2].
• Taurocholate caused a dose-dependent increase in mucin secretion, suggesting that bile salt was the bile component responsible for the stimulatory effect [7].

Other interactions of LOC442975

• The MUC1 gene product (PEM, polymorphic epithelial mucin) is a cell-associated glycoprotein expressed on the apical surface of most simple secretory epithelia [18].
• Exogenous tumor necrosis factor alpha (TNF-alpha) (1-10 ng/mL) did cause a minor increase in mucin secretion by the DGBE cells, but the effect of LPS from E. coli on mucin secretion could not be inhibited by preincubation with a TNF-alpha antibody (10 microg/mL) [4].
• In conclusion, our results suggested that the PGE2 induced by COX-2 might play a role in mucin secretion from the gallbladder epithelium through the increment of cAMP [19].
• Mucin assay and western blots for COX-1 and COX-2 were performed [19].
• Correlations were made after parenteral injection of secretin which increased movement of tantalum particles and production of mucin, and after injection of glucagon, which stopped movement of the particles and decreased mucin secretion in the pouch [20].

Analytical, diagnostic and therapeutic context of LOC442975

• An organ culture technique was used to measure mucin secretion in normal prairie dog gallbladder in response to exogenous prostaglandins and agents that increased or decreased endogenous prostaglandin production [2].
• A 7.8% +/- 1.7% increase in mucin above basal levels after 24 hours was observed with a solid-phase immunoassay in control wells, whereas histamine, gastrin, and carbamylcholine increased total mucin by 14% +/- 0.7%, 17% +/- 4.3%, and 20.4% +/- 4%, respectively (all P < 0.01), and PGE2 had no significant effect [8].
• In the present study, mucin production and release of the surface-active phospholipid phosphatidylcholine (PC) into the medium were measured with an isolated canine mucous cell culture system [8].
• We have examined the trafficking of the mucin-like protein endolyn in transfected, polarized MDCK cells using biochemical approaches and immunofluorescence microscopy [21].
• The translation products were analyzed by gel electrophoresis and fluorography before and after immunoprecipitation with the antiserum to deglycosylated mucin [22].

References