Acid stimulates E-cadherin surface expression on gastric epithelial cells to stabilize barrier functions via influx of calcium

Background and aims E-cadherin, which is a [Ca2+]-dependent, homotypic cell -cell adhesion molecule, is expressed in gastrointestinal epithelial cells. Much has been learned about the down-regulation of E-cadherin expression i n gastrointestinal tumours, Barrett's oesophageal dysplasia, and Crohn's di sease, but the functions of this molecule in normal gastrointestinal mucosa are less known. Methods In this study, we investigated the relationship between E-cadherin expression and permeability using rat cultured gastric and intestinal epith elial cells following a 30-min exposure to various pH solutions. We also in vestigated the participation of [Ca2+] in these events. Results E-cadherin expression increased under acid (pH 4) but not alkali (p H 10 or 11) exposure only for gastric epithelial cells. Gastric epithelial permeability was maintained only against acid exposure while intestinal per meability increased under both conditions. Transient influx of [Ca2+] was o nly observed for gastric epithelial cells just after acid exposure. Conclusions These findings suggest that E-cadherin expression on gastric ep ithelium stabilizes the epithelial barrier against acid, probably through i nflux of [Ca2+]. This event is thought to be one of the protective mechanis ms in gastric mucosa against acid back-diffusion, which is one of the cause s of peptic ulcer formation. Eur J Gastroenterol Hepatol 13:127-136 (C) 200 1 Lippincott Williams & Wilkins.