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Background —Treatment with an antibody that binds β3 integrins (abciximab; c7E3 Fab) at the time of coronary angioplasty decreases the need for repeat revascularization. Two potential mechanisms have been proposed to explain this effect: (1) inhibition of platelet aggregation or (2) interruption of ligand binding to β3 integrins on the smooth muscle cell (SMC) surface. We examined the latter hypothesis by determining (1) if β3 integrin expression is upregulated after vascular injury in the baboon, (2) if 7E3 binds β3 integrins on cultured SMC, and (3) if β3 integrin activation plays a role in proliferation of cultured SMC.Methods and Results —Results demonstrated that immunostaining for β3 integrins was present in the neointima 1 week after balloon withdrawal injury of baboon brachial arteries and that β3 integrin expression colocalized with α-actin–positive cells. In contrast, staining for β3 integrins was undetectable in contralateral uninjured brachial arteries. 7E3 bound to cultured human aortic SMC with an affinity (K D =3.3 nmol/L) similar to 7E3 binding to endothelial cells or platelets. Cotreatment with 7E3 partially inhibited thrombospondin-induced or α-thrombin–induced proliferation but not PDGF-induced or serum-induced proliferation.Conclusions —In summary, these studies demonstrate that vascular cell β3 integrin expression is increased after injury, that 7E3 binds to cultured SMC with high affinity, and that β3 activation is important for thrombospondin-induced or α-thrombin–induced proliferation. These results support the hypothesis that β3 integrins play a role in SMC growth responses after balloon injury.

circulation

β <sub>3</sub> Integrins Are Upregulated After Vascular Injury and Modulate Thrombospondin- and Thrombin-Induced Proliferation of Cultured Smooth Muscle Cells

β 3 Integrins Are Upregulated After Vascular Injury and Modulate Thrombospondin- and Thrombin-Induced Proliferation of Cultured Smooth Muscle Cells

β ₃ Integrins Are Upregulated After Vascular Injury and Modulate Thrombospondin- and Thrombin-Induced Proliferation of Cultured Smooth Muscle Cells