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Am J Physiol Lung Cell Mol Physiol (April 8, 2005). doi:10.1152/ajplung.00248.2004
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Submitted on July 2, 2004
Accepted on March 30, 2005

PKC-dependent, burn-induced adherens junction reorganization and barrier dysfunction in pulmonary microvascular endothelial cells

John H. Tinsley1*, Jerome W. Breslin2, Nicole R. Teasdale1, and Sarah Y. Yuan2

1 Department of Surgery, Scott and White Memorial Hospital; Scott, Sherwood and Brindley Foundation, Temple, TX, USA
2 Department of Surgery, University of California Davis Medical Center, Sacramento, CA, USA

* To whom correspondence should be addressed. E-mail: jht{at}tamu.edu.

Rat lung microvascular endothelial cell monolayers were exposed to donor plasma from burned rats (25% total body surface area) at a 1:3 dilution for 30 min. Immunofluorescence analysis revealed that concomitant with gap formation alterations were seen in the adherens junction (AJ) proteins B-catenin, and vascular endothelial (VE)-cadherin. Both of these components were shown to exist in a smooth, uniform arrangement at the cell periphery in untreated cells. However, upon exposure to burn plasma, this uniformity was lost and the AJ proteins showed a disrupted, zipper-like pattern at the cells' edge. In addition, these proteins were absent from areas of gap formation between the cells and an increase in punctate staining throughout the cells suggests they were internalized in response to burn plasma. Measurements of both transendothelial electrical resistance (TER) and FITC-albumin flux across the cell monolayer were used to assess barrier integrity. Our study found that exposure to burn plasma rapidly caused the electrical resistance across confluent monolayers to decrease and albumin flux to increase, phenomena associated with barrier dysfunction. Furthermore, all the above responses to burn plasma were attenuated when cells were pretreated with the PKC inhibitor bisindolylmaleimide, suggesting that protein kinase C is required for burn-induced pulmonary endothelial dysfunction.




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