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1 Division of Pulmonary and Critical Care Medicine, Keck School of Medicine, Will Rogers Institute Pulmonary Research Center, Los Angeles, CA, USA
2 Department of Anesthesiology Critical Care, Childrens Hospital Los Angeles, Los Angeles, CA, USA
3 Department of Molecular Pharmacology and Toxicology, University of Southern California, School of Pharmacy, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: zborok{at}usc.edu.
Rat alveolar epithelial type II (AT2) cells grown on polycarbonate filters form high resistance monolayers and concurrently acquire many phenotypic properties of type I (AT1) cells. Treatment with epidermal growth factor (EGF) has previously been shown to increase transepithelial resistance (TER) across alveolar epithelial cell (AEC) monolayers. We investigated changes in claudin expression in primary cultured AEC during transdifferentiation to the AT1 cell-like phenotype (days 0, 1 and 8), and on day 5 in culture +/- EGF (10 ng/ml) from day 0 or day 4. Claudins 4 and 7 were increased, while claudins 3 and 5 were decreased, on later compared with earlier days in culture. Exposure to EGF led to increases in claudins 4 and 7 and decreases in claudins 3 and 5. Claudin 1 was only faintly detectable in freshly isolated AT2 cells and remained unchanged over time in culture and following exposure to EGF. These results suggest that increases in TER accompanying AEC transdifferentiation and/or EGF exposure are mediated, at least in part, by changes in the pattern of expression of specific claudin isoforms.
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