Abstract
Smooth muscle cells (SMCs), present in the media layer of blood vessels, are crucial in maintaining vascular homeostasis. Upon vascular injury, SMCs show a high degree of plasticity, undergo a change from a “contractile” to a “synthetic” phenotype, and play an essential role in the pathophysiology of diseases including atherosclerosis and restenosis. Integrins are cell surface receptors, which are involved in cell-to-cell binding and cell-to-extracellular-matrix interactions. By binding to extracellular matrix components, integrins trigger intracellular signaling and regulate several of the SMC function, including proliferation, migration, and phenotypic switching. Although pharmacological approaches, including antibodies and synthetic peptides, have been effectively utilized to target integrins to limit atherosclerosis and restenosis, none has been commercialized yet. A clear understanding of how integrins modulate SMC biology is essential to facilitate the development of integrin-based interventions to combat atherosclerosis and restenosis. Herein, we highlight the importance of integrins in modulating functional properties of SMCs and their implications for vascular pathology.
Highlights
Vascular smooth muscle cells (SMCs), present in the media layer of arteries, are critical to maintain the vascular tone of resistance arteries through synergic action between vasodilators/vasoconstrictors and vascular SMC contractility
The transition of SMCs from a “contractile” to a “synthetic” phenotype is known as SMC phenotypic modulation or switching, which contributes to SMC proliferation, and migration, and thereby plays a vital role in the progression of atherosclerosis, in-stent restenosis, and other cardiovascular hyperplastic disorders
Expressed in normal SMCs, and upregulated in SMCs cultured on fibronectin and during neointimal hyperplasia highly abundant in cultured SMCs, upregulated upon vascular injury promote chemotaxis of arterial SMCs α2β1 deletion had no effect on atherosclerosis
Summary
Vascular smooth muscle cells (SMCs), present in the media layer of arteries, are critical to maintain the vascular tone of resistance arteries through synergic action between vasodilators/vasoconstrictors and vascular SMC contractility. SMCs are not terminally differentiated and have the flexibility to shift from a contractile to a proliferative, pro-migratory, synthetic phenotype, exhibiting a rhomboid morphology. These de-differentiated SMCs are characterized by reduced expression of contractile proteins [2]. SMC phenotype [3,4,5,6] These dedifferentiated SMCs re-enter the cell cycle and secrete ECM components, including fibronectin, which contributes to vascular remodeling. The adhesion, proliferation, and migration of SMCs are regulated by the interaction of integrins with ECM components [10]
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