{'fraction_non_alphanumeric': 0.01569995638901003, 'fraction_numerical': 0.0065416484954208464, 'mean_word_length': 5.766961651917404, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Protective actions of rat gastric epithelial E-cadherin expression against epithelial barrier dysfunctions induced by chemical hypoxia–reoxygenation in vitro

Background and aim E-cadherin expressed on gastric epithelium is reported to form adherence junctions and stabilize barrier functions. While hypoxia–reoxygenation is well known to cause gastric mucosal injury during reoxygenation, gastric E-cadherin actions against this stress remain unclear. In this study, using the oxygen depleting agent thioglycolic acid we examined whether E-cadherin expressed on rat cultured gastric epithelial cells has protective actions against epithelial barrier dysfunction induced by chemical hypoxia–reoxygenation. Methods Chemical hypoxia was induced by incubating cells with 5 mm thioglycolic acid in glucose free medium for 60 min. Cells were then reoxygenated for 240 min by changing to normal medium. The expression of E-cadherin on the cell surface was measured with an enzyme immunoassay, and epithelial permeability was determined by the diffusion rate of FITC–dextran through the cell layer. Results E-cadherin expression increased during the 60 min hypoxic period, accompanied by activation of protein kinase C, protein kinase G and protein kinase A. The increased expression significantly diminished, but was considerably higher than the control values during reoxygenation for 180 min, which was partially due to generation of reactive oxygen species but not to activation of protein kinase. Conversely, epithelial permeability was stabilized during hypoxia, but increased only for 30 min of reoxygenation, probably due to generation of reactive oxygen species. Epithelial permeability during hypoxia was elevated by a combination of all the protein kinase inhibitors. Conclusion An increase in the expression of E-cadherin during hypoxia through the activation of the kinases is likely to stabilize epithelial barrier functions. The reactive oxygen species generated during 30 min reoxygenation increased the molecular expression of E-cadherin less than during hypoxic stress. The transient break in the barrier functions caused by reactive oxygen species during reoxygenation appears to overcome the reactive oxygen species mediated cytoprotective action increasing E-cadherin expression.