The well-being of an entire organism is dependent upon its vascular system, which transports oxygen, nutrients and hormones, and removes carbon-dioxide and other metabolic end products from tissues. The basement membrane of the arterial wall is composed mainly of extracellular matrix (ECM) molecules. By interacting with a family of cell adhesion receptors called integrins, ECM molecules provide structural support, and stimulate both physical and chemical signaling. Integrin-mediated signaling in either direction can regulate various aspects of vascular cell behavior, including their migratory ability, proliferation and wound repair. Extensive injury or inflammation to the vascular endothelium can compromise the ability of vascular cells to repair a wound. For example, injured endothelium could expose cell-binding epitopes that can promote adhesion of monocytes. Attached monocytes migrate through the endothelial cell (EC) junctions, into the sub-endothelial space via a complex mechanism and differentiate into macrophages. Moreover, specific ECM molecules encountered by vascular smooth muscle cells (vSMCs) following vascular wall injury could transform these cells to either “contractile” or “synthetic” phenotypes. Advances made in our understanding of integrin signaling that regulates contractile versus synthetic phenotypes of vSMC will be the subject of this review.
Keywords: Basement membrane, endothelial cells, extracellular matrix molecules, inflammation, injury, integrins, vascular smooth muscle cells, signaling
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