Identification of laminin receptor in gingival tissue and its interaction with tooth cementum laminin.

1. A gingival epithelial cell surface receptor for laminin was isolated from bovine gingival tissue by affinity chromatography on laminin. 2.

Protection against alcohol-induced gastric mucosal injury by nitecapone.

1. The mechanism of gastric mucosal protection by an anticular agent, nitecapone, against injury was investigated in rats with and without indomethacin pretreatment. 2.

Role of sulphation in post-translational processing of rat salivary mucins.

Segments of rat submandibular salivary gland were incubated in MEM supplemented with 10-800 microM sulphate in the presence of [3H]-glucosamine, [3H]-proline and [35S]-Na2SO4, with 0-8 mM chlorate, an inhibitor of 3'-phosphoadenosine-5'-phosphosulphate formation. Incorporation of glucosamine and sulphate depended upon the sulphate content of the medium and reached a maximum at 400 microM sulphate. The introduction of chlorate into the medium, while having no effect on the protein synthesis as shown by [3H]-proline incorporation, caused, at its optimal concentration of 4 mM, a 90% decrease in mucin sulphation and a 29% drop in mucin glycosylation.

Effect of ethanol on epidermal growth factor receptor in buccal mucosa.

The effect of ethanol on buccal mucosal epidermal growth factor receptors was investigated. The buccal mucosal cells from adult rats were incubated in DMEM at 4 degrees C and 37 degrees C in the presence of various concentrations (0-5%) of ethanol and then assayed for EGF receptor binding using [125I]-EGF. The results of binding analysis showed that the cells incubated in the presence of ethanol displayed diminished [125I]-EGF binding.

Prostaglandin E2 receptor of rat submandibular salivary glands.

The binding characteristics of the PGE2 receptor were investigated in membrane preparations from these glands. Specific [3H]PGE2 binding was linear as a function of the membrane protein concentration and reached steady state by 40 min of incubation at 37 degrees C under neutral pH. Scatchard analysis of the binding data produced a curvilinear plot with a Kd of 0.

Adrenergic and cholinergic regulation of phospholipid release in sublingual salivary gland in vitro.

1. The role of adrenergic and cholinergic mediators in the regulation of salivary phospholipid secretion was investigated using rat sublingual acinar cells maintained in the presence of [3H]choline. 2.

Enhancement in gastric mucus gel qualities with colloidal bismuth subcitrate administration.

The effects of intragastric administration of an antiulcer drug, colloidal bismuth subcitrate, on the content, composition and physical properties of the mucus component of gastric mucosal barrier were investigated. The experiments were conducted with two groups of rats in which one group received twice daily for three consecutive days a dose of 100 mg/kg colloidal bismuth subcitrate, while the control group received saline. The animals were killed 16 h after the last dose, their stomachs dissected and the mucosa subjected to physicochemical measurements.

Participation of phosphoinositides in gastric mucosal protection by colloidal bismuth subcitrate against ethanol-induced injury.

The mechanism of gastric mucosal protection by an antiulcer agent, colloidal bismuth subcitrate (CBS), against ethanol-induced injury was investigated using in vivo and in vitro systems. The experiments in vivo were conducted with groups of rats with and without indomethacin pretreatment, and the animals received either a dose of CBS (100 mg/kg) or a vehicle (saline), followed 30 min later by ethanol. In the in vitro studies, gastric mucosa segments were cultured in the presence of CBS, ethanol, or both.

Colloidal bismuth subcitrate inhibits peptic degradation of gastric mucus and epidermal growth factor in vitro.

The effect of an antiulcer drug, colloidal bismuth subcitrate (De-Nol), on the proteolytic activity of pepsin toward gastric mucus and salivary epidermal growth factor was investigated. Samples of pig gastric mucus and mouse epidermal growth factor were incubated with pepsin in the absence and in the presence of De-Nol, and the released alpha-amino acid residues were quantified. Results of analysis revealed that, in the absence of De-Nol, the apparent Km value of pepsin toward gastric mucus was 1.

Purification of protein fatty acyltransferase and determination of its distribution and topology.

Studies reported from this laboratory have demonstrated that O-glycosidic glycoproteins of salivary, pulmonary, and gastrointestinal origin are acylated by fatty acyltransferase residing in Golgi and microsome-enriched fraction (Slomiany, A., Liau, Y.H.

Characterization of epidermal growth factor receptor in rat buccal mucosal cells.

1. Receptor binding for epidermal growth factor (EGF) in rat buccal mucosa was characterized. Binding of [125I]EGF to rat buccal mucosa was time, temperature, cell number and [125I]EGF concentration dependent.

Effect of lipids on the lactic acid retardation capacity of tooth enamel and cementum pellicles formed in vitro from saliva of caries-resistant and caries-susceptible human adults.

The lipid content and composition of these pellicles and the effect of lipids on their ability to retard the diffusion of lactic acid were investigated. Lipids accounted for 22.4% of the dry weight of caries-resistant enamel pellicle and 19.

Identification of epidermal growth factor receptor in human buccal mucosa.

EGF receptor was identified and its binding characteristics were determined. Buccal mucosa was obtained from 12 healthy volunteers (6 males and 6 females) and assayed individually for [125I]-EGF binding. The specific binding of [125I]-EGF to the receptor ranged from 2.

Sucralfate protection of gastric mucosa against alcohol-induced injury: a phosphoinositide mediated process.

The mechanism of protection by sucralfate against gastric mucosal injury induced by ethanol was investigated. The experiments in vivo were conducted with groups of rats with and without indomethacin pretreatment, and the animals received sucralfate followed by ethanol. In the in vitro experiments, gastric mucosa was cultured in the presence of sucralfate, ethanol, or both.

Characterization of gastric mucosal prostaglandin E2 receptor.

1. The binding characteristics of gastric mucosal prostaglandin (PG) E2 (PGE2) receptor were investigated using mucosal cell membranes from rat stomach. The binding was found to be dependent upon PGE2 and membrane protein concentration, the time of incubation and the pH of the mixture, being highest at pH 3.

Characterization of the epidermal growth factor receptor in the gastric mucosa.

The effects of epidermal growth factor (EGF), a potent mitogen involved in mucosal protection, are mediated by specific cellular receptors. Here, we present the characteristics and binding properties of EGF receptors in the gastric mucosa. The studies were conducted using cell membranes isolated by subcellular fractionation of rat stomach mucosal scrapings.

Gastric mucosal protection by sucralfate involves phosphoinositides participation.

1. The mechanism of gastroprotective action of an antiulcer drug, sucralfate, was investigated. Studies in vivo were conducted with groups of rats with and without indomethacin pretreatment, and the animals received sucralfate followed by ethanol.

The relationship of prostaglandins to cAMP, IgG, IgM and alpha-2-macroglobulin in gingival crevicular fluid in chronic adult periodontitis.

Gingival crevicular fluid, collected from 8 patients with chronic adult periodontitis before and 21 days after root planing and scaling, was analysed for prostaglandin E2, 6KPGF1 alpha, cAMP, IgG, IgM and alpha-2-macroglobulin, and their inter-relationship evaluated. There was a significant decrease in the levels of prostaglandin E2, IgG, IgM and alpha-2-macroglobulin after treatment, whereas the levels of 6KPGF1 alpha and cAMP remained essentially unchanged. The level of prostaglandin E2 decreased by 35%, IgG by 32%, IgM by 90%, and alpha-2-macroglobulin by 79%.

Lipolytic activity of Campylobacter pylori: effect of colloidal bismuth subcitrate (De-Nol).

Infection by Campylobacter pylori appears to play a major role in the etiology of gastric disease, but the nature of impairment evoked by this pathogen in gastric mucosal defense is not well understood. We present here evidence that the extracellular material elaborated by this microorganism exhibits lipolytic activity capable of gastric mucosal lipid degradation. The colonies of bacteria, cultured from antral mucosal biopsy specimens of patients undergoing endoscopy, were washed with saline, passed through a sterilization filter, and the filtrate was examined for lipase and phospholipase activities.

Campylobacter pylori colonization factor shows specificity for lactosylceramide sulfate and GM3 ganglioside.

The specificity of Campylobacter pylori cell surface lectin, a presumptive colonization factor, was investigated using various sulfated and sialic acid containing glycolipids. C. pylori cells, cultured from human antral mucosal biopsies, were incubated with intact and modified glycolipid preparations and examined for agglutination inhibition of human erythrocytes.

Colloidal bismuth subcitrate (De-Nol) inhibits degradation of gastric mucus by Campylobacter pylori protease.

There is increased awareness that infection with Campylobacter pylori could be a major factor in the pathogenesis of gastric disease. Here, we present evidence that the extracellular protease elaborated by this bacteria, which causes degradation of gastric mucus, is inhibited by an antiulcer agent, colloidal bismuth subcitrate (CBS; De-Nol). The study was conducted with C.

Synthesis and initial processing of gastric apomucin.

The initiation of the processing of apomucin was investigated using mucus glycoprotein synthesizing polysomes from rat gastric epithelial cells. The polysomes were isolated from cells labeled with [3H]palmitic acid and [14C]N-acetylgalactosamine, purified on Helix pomatia-Sepharose affinity column, dissociated to release peptidyl-tRNA, and chromatographed on DEAE-HPLC column to separate peptidyl-tRNA complexes from the free and ribosomal RNA and proteins. The analysis of the HPLC purified peptidyl-tRNA revealed that complexes were labeled with [3H]palmitic acid and [14C]N-acetylgalactosamine.

In vitro sulfation of sublingual salivary gland mucin: structures of 35S-labeled oligosaccharides.

The enzyme which catalyzes the transfer of sulfate ester group from 3'-phosphoadenosine-5'-phosphosulfate to salivary mucus glycoprotein was located in the detergent extract of the Golgi-rich membrane fraction of rat sublingual salivary glands. Alkaline borohydride reductive cleavage of the synthesized 35S-labeled glycoprotein led to the liberation of the label into the reduced acidic oligosaccharide fraction. A 90.

Lipolytic activity of Campylobacter pylori: effect of sofalcone.

The lipolytic activity of Campylobacter pylori capable of gastric mucosal lipid degradation was investigated. The colonies of bacteria, cultured from antral mucosal biopsy specimens of patients undergoing endoscopy, were washed with saline and passed through a sterilization filter; the filtrate was examined for lipase and phospholipase A activities, using glycerol trioleate and dipalmitoyl phosphatidylcholine as substrates. The obtained results revealed that both enzymes are present in the C.

Enzymatic sulfation of mucus glycoprotein in rat submandibular salivary gland.

1. The enzymic activity which catalyzes transfer of sulfate ester group from 3'-phosphoadenosine-5'-phosphosulfate to mucus glycoprotein was found associated with Golgi-rich membrane fraction of rat submandibular salivary gland. 2.