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Published ahead of print on January 23, 2003, doi:10.1165/rcmb.2002-0180OC

Am. J. Respir. Cell Mol. Biol., Volume 29, Number 1, July 2003, 62-70

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Submitted on September 4, 2002
Revised on January 17, 2003

Heterogeneity of claudin expression by alveolar epithelial cells

Fushan Wang1, Brandy Daugherty1, Lisa L Keise1, Zhangyong Wei2, Joseph P Foley3, Rashmin C Savani4, and Michael Koval1*

1 Physiology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA; Institute for Environmental Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA, 2 Physiology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA, 3 Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, PA, USA, 4 Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, PA, USA; Institute for Environmental Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA

* To whom correspondence should be addressed. E-mail: mkoval{at}mail.med.upenn.edu.

Claudins are proteins that participate in epithelial barrier function and regulate paracellular permeability. By immunohistochemistry of adult rat lung sections, claudin-3, claudin-4 and claudin-5 were found to be co-expressed by type II alveolar epithelial cells. Claudin-3 and claudin-4 were also co-expressed by some alveolar epithelial cells adjacent to type II cells. In contrast, claudin-5 was expressed throughout the alveolus. Isolated primary rat alveolar epithelial cells in culture also expressed claudin-3, claudin-4 and claudin-5, but showed little claudin-1 and claudin-2 expression. Claudin expression by isolated cells at both the mRNA and protein level varied with time in culture. In particular, claudin-3 and claudin-5 co-localized and were distributed around the alveolar cell periphery, but claudin-4 expression was heterogeneous. We also found that paracellular permeability was increased when cultured alveolar epithelial cells were treated with a fatty acid amide, methanandamide. Methanandamide did not alter cell viability and had little effect on the localization of claudin-3, claudin-4, claudin-5, occludin or ZO-1, suggesting that localization of these proteins to cell-cell contact sites is not sufficient for maintaining barrier function. However, methanandamide-treated cells showed a 12-fold increase in claudin-5 expression and a 2-3 fold increase in claudin-3, consistent with the notion that specific changes in claudin expression levels may correlate with changes in alveolar epithelial barrier function.




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