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Apical and basolateral EGF receptors regulate gastric mucosal paracellular permeability
M C Chen1, J Goliger, N Bunnett
1CURE: Digestive Diseases Research Center, West Los Angeles Veterans Affairs Medical Center, School of Medicine, University of California, Los Angeles 70073, California. mcychen@ucla.edu
American Journal of Physiology. Gastrointestinal and Liver Physiology
|February 24, 2001
Summary
Epidermal growth factor (EGF) regulates canine gastric epithelial cell permeability. Apical and basolateral EGF receptors (EGFR) activate signaling pathways, with sustained apical EGFR activation potentially key for regulating cell barrier function.
Area of Science:
- Cell Biology
- Epithelial Physiology
- Gastroenterology
Background:
- Canine oxyntic epithelial cells form resistant monolayers.
- Previous studies noted mitogenic and migratory responses to epidermal growth factor (EGF).
Purpose of the Study:
- Investigate EGF's effect on canine gastric epithelial cell monolayers.
- Determine the role of apical and basolateral EGF receptors (EGFR) in regulating paracellular permeability and cellular signaling.
Main Methods:
- Primary culture of canine oxyntic epithelial cells.
- Measurement of transepithelial resistance (TER) and short-circuit current.
- Mannitol flux assays to assess paracellular permeability.
- EGF binding assays and confocal microscopy for receptor localization and downstream signaling (tyrosine phosphorylation).
Main Results:
- EGF increased TER and decreased mannitol flux, indicating regulation of paracellular permeability.
- Both apical and basolateral EGF activated EGFR, beta-catenin, and cellular substrates.
- Apical EGFR activation led to a sustained increase in TER, while basolateral activation was transient.
- Despite lower apical receptor numbers, apical EGF triggered prominent beta-catenin phosphorylation.
Conclusions:
- Functional apical and basolateral EGFR are present on canine gastric epithelial cells.
- EGFR activation regulates paracellular permeability.
- Sustained apical EGFR signaling and beta-catenin phosphorylation suggest a critical role for apical EGFR in maintaining epithelial barrier integrity.