Journal
JOURNAL OF APPLIED PHYSIOLOGY
Volume 98, Issue 1, Pages 322-328Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00681.2004
Keywords
epidermal growth factor; tight junctions; transepithelial resistance; monolayer
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Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R37HL038578, R21HL072231, R01HL062569, R37HL062569, R01HL038578, R01HL038658, R01HL038621, R01HL064365] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [R01DE010742] Funding Source: NIH RePORTER
- NHLBI NIH HHS [HL 62569, HL 72231, HL 64365, HL 38658, HL 38621, HL 38578] Funding Source: Medline
- NIDCR NIH HHS [DE 10742] Funding Source: Medline
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Rat alveolar epithelial type II cells grown on polycarbonate filters form high-resistance monolayers and concurrently acquire many phenotypic properties of type I cells. Treatment with EGF has previously been shown to increase transepithelial resistance across alveolar epithelial cell (AEC) monolayers. We investigated changes in claudin expression in primary cultured AEC during transdifferentiation to the type I 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, whereas 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 type II cells and remained unchanged over time in culture and after exposure to EGF. These results suggest that increases in transepithelial resistance 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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