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Transforming growth factor alpha and epidermal growth factor in protection and healing of gastric mucosal injury.
Pretreatment with indomethacin decreased in part the protection by TGF and EGF against ethanol-induced damage and virtually abolished the protective action of these peptides against stress-induced injury. Expand
Role of endothelin-1 and constitutive nitric oxide synthase in gastric mucosal resistance to indomethacin injury: effect of antiulcer agents.
It is suggested that an increase in the vasoconstrictive ET-1 level combined with a decrease in regulatory cytokine, IL-4, and a loss of compensatory action by cNOS may be responsible for the gastric mucosal injury caused by indomethacin. Expand
Src-kinase-dependent epidermal growth factor receptor transactivation in salivary mucin secretion in response to β-adrenergic G-protein-coupled receptor activation
The findings underline the role of EGFR as a convergence point in modulation of salivary mucin secretion triggered by β-adrenergic agonist GPCR activation and demonstrate the importance of Src kinase in the EGFR transactivation process. Expand
Isolation and structural studies of sulfated glycoproteins of hog gastric mucosa.
The carbohydrate chains of the sulfated glycoproteins from hog stomach mucosa are linked to the protein through O-glycosidic bonds involving N-acetylgalactosamine and serine and threonine and some of the linkages between the sugars. Expand
Structures of the neutral oligosaccharides isolated from A-active human gastric mucin.
Alkaline borohydride reductive cleavage of the mucin, purified from gastric aspirates of the secretors with blood group A, resulted in a heterogeneous population of neutral (79.7%) and acidic (20.3%)Expand
Structural characterization of neutral oligosaccharides of human H+Leb+ gastric mucin.
The structure of carbohydrate chains of human gastric mucin was investigated and the following structures were proposed: mono-, bi-, and triantennary structures, based on hemagglutination inhibition data in H- anti-H, Leb-anti-Leb, and I- Anti-I systems. Expand
Salivary mucins in oral mucosal defense.
The salivary sulfo- and sialomucins actively participate in the modulation of the oral mucosal calcium channel activity through the inhibition of EGF-stimulated channel protein tyrosine phosphorylation, which is of paramount importance to mucosalcium homeostasis. Expand
Retardation of hydrogen ion diffusion by gastric mucus constituents: effect of proteolysis.
The results show that the ability of gastric mucus to retard the diffusion of hydrogen ion depends upon the polymeric structure of undegraded mucus glycoprotein and the extent of interaction of this glycop protein with lipids, serum albumin, and secretory IgA. Expand
Induction of tumor necrosis factor-alpha and apoptosis in gastric mucosal injury by indomethacin: effect of omeprazole and ebrotidine.
The findings provide new insights into the mechanism of gastric injury caused by NSAIDs and show that ebrotidine protection against indomethacin-induced mucosal damage occurs through the inhibition of epithelial cell apoptosis triggered by the enhancement in the mucosal TNF-alpha expression. Expand
Inhibition of gastric mucosal laminin receptor by Helicobacter pylori lipopolysaccharide: effect of nitecapone.
The results demonstrate that H. pylori is capable of disrupting gastric mucosal integrity by interfering with epithelial cell-laminin binding, and that an antiucler agent, nitecapone, counteracts this effect. Expand