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Background  The use of abciximab (c7E3 Fab) or eptifibatide improves clinical outcomes in diabetics undergoing percutaneous coronary intervention. These β 3  integrin inhibitors antagonize fibrinogen binding to α IIb β 3  integrins on platelets and ligand binding to α v β 3  integrins on vascular cells. α v β 3  integrins influence responses to insulin in various cell types but effects in human aortic smooth muscle cells (HASMC) are unknown.    Results and discussion  Insulin elicited a dose-dependent proliferative response in HASMC. Pretreatment with m7E3 (an anti-β 3  integrin monoclonal antibody from which abciximab is derived), c7E3 or LM609 inhibited proliferative responses to insulin by 81%, 59% and 28%, respectively. Eptifibatide or cyclic RGD peptides completely abolished insulin-induced proliferation whereas tirofiban, which binds α IIb β 3  but not α v β 3 , had no effect. Insulin-induced increases in c-Jun NH 2 -terminal kinase-1 (JNK1) activity were partially inhibited by m7E3 and eptifibatide whereas antagonism of α v β 3  integrins had no effect on insulin-induced increases in extracellular signal-regulated kinase (ERK) activity. Insulin stimulated a rapid increase in the number of vinculin-containing focal adhesions per cell and treatment with m7E3, c7E3 or eptifibatide inhibited insulin-induced increases in focal adhesions by 100%, 74% and 73%, respectively.    Conclusion  These results demonstrate that α v β 3  antagonists inhibit signaling, focal adhesion formation and proliferation of insulin-treated HASMC.

Eptifibatide and abciximab inhibit insulin-induced focal adhesion formation and proliferative responses in human aortic smooth muscle cells