[Frontiers in Bioscience 16, 644-673, January 1, 2011]

Regulation of VSMC behavior by the cadherin-catenin complex

Cressida Lyon, Carina Mill, Aikaterini Tsaousi, Helen Williams, Sarah George

Bristol Heart Institute, University of Bristol, Research Floor Level Seven, Bristol Royal Infirmary, Upper Maudlin St, BRISTOL, BS2 8HW, United Kingdom

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. The cadherin:catenin complex
3.1. The cadherin structure
3...2.The beta-catenin Wnt pathway
3.3. Wnt pathway inhibitors
4. Role of cadherin:catenin complex in regulation of VSMC behaviour
4.1. Role of the cadherin:catenin complex in the regulation of VSMC proliferation
4.2. Role of the cadherin:catenin complex in the regulation of VSMC migration
4.3. Role of the cadherin:catenin complex in the regulation of VSMC apoptosis
4.3.1. N-cadherin
4.3.2. Soluble N-cadherin
4.3.3. Beta-catenin
5. Evidence for the involvement of cadherin-beta-catenin complex and Wnts in human atherosclerosis, intimal thickening and aneurysms
6. Summary
7. Acknowledgement
8. References

1. ABSTRACT

Vascular smooth muscle cells (VSMCs) are the predominant cell type within blood vessels. In normal vessels VSMC have low rates of proliferation, migration and apoptosis. However, increased VSMC proliferation, migration, and apoptosis rates radically alter the composition and structure of the blood vessel wall and contribute to vascular diseases such as atherosclerosis, in-stent restenosis and vein graft failure. Consequently, therapies that modulate VSMC proliferation, migration and apoptosis may be useful for treating vascular diseases. In this review article we discuss recently emerging research that has revealed that homophilic cell-cell contacts mediated by the cadherin:catenin complex and Wnt/beta-catenin signalling are important regulators of VSMC behaviour.