Role of E-cadherin in the Pathogenesis of Gastroesophageal Reflux Disease

An early event in the pathogenesis of gastroesophageal reflux disease (GERD) is an acid-induced increase in junctional (paracellular) permeability in esophageal epithelium (EE). The molecular events that account for this change are unknown. E-cadherin is a junctional protein important in barrier function in EE. Therefore, defects in barrier function in EE were sought in GERD as well as whether their presence correlated with abnormalities in e-cadherin

Effects of ethanol and extract of cigarette smoke on the rabbit buccal mucosa

WOS: 000285881100005PubMed ID: 20923442Aim: The combination of smoking and drinking alcohol has a high association with diseases of squamous epithelium within the human oral cavity. Therefore, a study was done to assess the impact of these agents alone or in combination on the squamous epithelium using as model the buccal epithelium from rabbit oral cavity. Methods: Buccal epithelium was mounted in Ussing chambers to monitor electrical parameters during exposure to ethanol (5-40%) or to Ringer extract of cigarette smoke (EOCS) from one to six cigarettes dissolved in 10 ml Ringer either alone or with combination. Results: Exposure to EOCS reduced in a dose dependent manner above 2 cigarettes/10 ml transmural electrical potential difference (PD), short-circuit current (I-sc), increased transmural electrical resistance (R). Morphology showed from generalize tissue edema to patchy necrosis with the increasing concentrations. Ethanol alone raised PD, I-sc and R at lower concentrations (5%) and lowered PD, I-sc and R at higher concentrations (40%). The combination of 5% ethanol, EOCS-1cigarette/10 ml reduced PD, I-sc by 58% and increased R by 29%. Unlike exposure to 5% EtOH and EOCS-1, 10% EtOH combined with EOCS-1 produces a harmful effect by dropping PD and I-sc. Conclusion: Both, simultaneous, and sequential, use of these agents enhanced their negative impact on these parameters. The enhancement of these effects are not due to solubulization of additional tobacco products by EtOH or by or by EtOH enhancing smoking noxious effect. Histopathologic damage needs higher concentrations of ethanol and EOCS combination and changes were more profound compared to the sum of the isolated effects of both agents.National Institutes of HealthUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [R01-DK36013]This study is supported by National Institutes of Health grant R01-DK36013