Reduction of E-cadherin by human defensin-5 in esophageal squamous cells

摘要: Barrett's esophagus (BE) is metaplastic columnar epithelium converted from normal squamous epithelia in the distal that thought to be a precancerous lesion of esophageal adenocarcinoma. BE attributed gastroesophageal reflux disease (GERD), and therefore gastric acid or bile acids are factors cause epithelial cell damage inflammation gastro-esophageal junction. The decrease adherent junction molecules, E-cadherin has been reported associated with progression carcinoma, but initiation not sufficiently understood. characterized by presence goblet cells occasionally Paneth observed at base crypts. possess dense granules, which human antimicrobial peptide defensin-5 (HD-5) stored secreted out cells. This study determined roles HD-5 produced against adjacent A line Het-1A, was incubated synthetic as model junctions, alterations were investigated. Immunocytochemistry, flowcytometry, Western blotting showed expression protein decreased. And partial recovery treatment CD10/neprilysin inhibitor (thiorphan). In conclusion, reduced using vitro experiments. junction, may accelerate BE.