Adhesion and migration of smooth muscle cells during atherosclerotic plaque formation.
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During the initiation and progression of atherosclerosis, migration and proliferation of vascular smooth muscle cells (VSMCs) play important roles in lesion formation. Contractile VSMCs are adhesive and play a role in the contractile function of the artery. These cells can differentiate into synthetic VSMCs upon injury, gaining the ability to migrate and proliferate. This phenotype switch is accompanied by differential expression of several adhesion molecules that are involved in cell-cell binding or cell-extracellular matrix interactions. The adhesion molecules discussed in this thesis include the four major families of adhesion molecules: integrins, cadherins, selectins and immunoglobulin superfamily cell adhesion molecules. Members of these families of adhesion molecules were shown to play a role in VSMCs migration, and thereby the formation of an atherosclerotic lesion. This thesis focuses on the role of adhesion molecules during phenotype switching, and the migration of VSMCs during arterial injury.