Role of calpain in platelet adhesion and spreading. (A) Levels of FAK and PYK2 in washed platelets from healthy subjects (CTL) and from patients with type 2 diabetes (Diab/D) and activated μ- and m-calpain. (B) FAK, PYK2, and ILK are calpain substrates in vitro. Washed human platelets were treated with either solvent or ionomycin in the absence (Sol) and presence of calpeptin (Cpt, 10μM). (C) Adherence of human platelets pre-treated with and without Ca²⁺ in the absence or in the presence of calpeptin (Cpt) to fibronectin-coated slides. (D) Adherence of platelets from μ-cal^fl/fl or PF4-μ-Cal^−/− mice pretreated with and without Ca²⁺ in the absence or in the presence of calpeptin (Cpt). (E) Effect of calpain inhibition on numbers of activated and spread platelets after stimulation of washed platelets from μ-cal^fl/fl and PF4-μ-Cal^−/− mice with Ca²⁺ in the absence or in the presence of calpeptin (Cpt). The graphs summarize data obtained in platelets from 4-5 subjects or 6-9 animals per group. *P < .05; **P < .01 versus control; #P < .05 versus Ca²⁺-stimulated platelets without calpeptin.