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. 2002 Sep;283(3):C811-21.
doi: 10.1152/ajpcell.00417.2001.

Regulation of endothelial barrier function and growth by VE-cadherin, plakoglobin, and beta-catenin

Kala Venkiteswaran  1 , Kanyan Xiao, Susan Summers, Cathárine C Calkins, Peter A Vincent, Kevin Pumiglia, Andrew P Kowalczyk
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Free article

Regulation of endothelial barrier function and growth by VE-cadherin, plakoglobin, and beta-catenin

Kala Venkiteswaran et al. Am J Physiol Cell Physiol. 2002 Sep.
Free article

Abstract

VE-cadherin is an endothelial-specific cadherin that plays a central role in vascular barrier function and angiogenesis. The cytoplasmic domain of VE-cadherin is linked to the cytoskeleton through interactions with the armadillo family proteins beta-catenin and plakoglobin. Growing evidence indicates that beta-catenin and plakoglobin play important roles in epithelial growth and morphogenesis. To test the role of these proteins in vascular cells, a replication-deficient retroviral system was used to express intercellular junction proteins and mutants in the human dermal microvascular endothelial cell line (HMEC-1). A mutant VE-cadherin lacking an adhesive extracellular domain disrupted endothelial barrier function and inhibited endothelial growth. In contrast, expression of exogenous plakoglobin or metabolically stable mutants of beta-catenin stimulated HMEC-1 cell growth, which suggests that the beta-catenin signaling pathway was active in HMEC-1 cells. This possibility was supported by the finding that a dominant-negative mutant of the transcription factor TCF-4, designed to inhibit beta-catenin signaling, also inhibited HMEC-1 cell growth. These observations suggest that intercellular junction proteins function as components of an adhesion and signaling system that regulates vascular barrier function and growth.

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