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Am J Physiol Cell Physiol 280: C1657-C1668, 2001;
0363-6143/01 $5.00
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Vol. 280, Issue 6, C1657-C1668, June 2001

SPECIAL TOPIC
Etk/Bmx activation modulates barrier function in epithelial cells

Sarah F. Hamm-Alvarez1,3, Allen Chang2,*, Yanru Wang1,*, Galina Jerdeva1, H. Helen Lin2, Kwang-Jin Kim2,3,4,5,6, and David K. Ann2,7

Departments of 1 Pharmaceutical Sciences, 2 Molecular Pharmacology and Toxicology, 3 Physiology and Biophysics, 4 Biomedical Engineering, and 5 Medicine, 6 Will Rogers Institute Pulmonary Research Center, and 7 Center for Craniofacial Molecular Biology, University of Southern California, Los Angeles, California 90033

Etk/Bmx is a member of the Tec family of cytoplasmic non-receptor tyrosine kinases known to express in epithelial cells. We demonstrate herein that Etk activation in stably Etk-transfected epithelial Pa-4 cells resulted in a consistently increased transepithelial resistance (TER). After 24 h of hypoxic (1% O2) exposure, the TER and equivalent active ion transport rate (Ieq) were reduced to <5% of the normoxia control in Pa-4 cells, whereas both TER and Ieq were maintained at comparable and 60% levels, respectively, relative to their normoxic controls in cells with Etk activation. Moreover, Pa-4 cells exhibited an abundant actin stress fiber network with a diffuse distribution of beta -catenin at the cell periphery. By contrast, Etk-activated cells displayed a redistribution of actin to an exclusively peripheral network, with a discrete band of beta -catenin also concentrated at the cell periphery, and an altered occludin distribution profile. On the basis of these findings, we propose that Etk may be a novel regulator of epithelial junctions during physiological and pathophysiological conditions.

signal transduction; adaptive response

* A. Chang and Y. Wang contributed equally to this work.




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