Open AccessRole of E-cadherin in the Pathogenesis of Gastroesophageal Reflux Disease
Author(s) -
Biljana Jovov,
Jianwen Que,
Nelia A. Tobey,
Zorka Djukic,
Brigid L.M. Hogan,
Roy C. Orlando
Publication year - 2011
Publication title -
the american journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.907
H-Index - 252
eISSN - 1572-0241
pISSN - 0002-9270
DOI - 10.1038/ajg.2011.102
Subject(s) - gerd , western blot , pathogenesis , medicine , esophagus , reflux , immunostaining , pathology , endocrinology , gastroenterology , immunohistochemistry , biology , disease , biochemistry , gene
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.