Figure 6
Figure 6. Reversal of the diabetes-associated calpain overactivation by in vivo calpain inhibition. (A) ILK, septin-5, FAK, and PYK2 levels in platelets from healthy (CTL) and streptozotocin-induced diabetic mice (Dia) treated with vehicle or the calpain inhibitor A-705253 (A70). (B) CCL5 in microparticles isolated from the plasma of healthy (CTL) or diabetic (Dia) mice treated with vehicle or A-705253. (C) Effect of in vivo A-705253 treatment on thrombus size after FeCl3-induced injury of carotid arteries from healthy (top panel) and diabetic (bottom panel) mice. (D) Number of circulating platelet-leukocyte aggregates in healthy (CTL) and diabetic (Dia) mice treated with vehicle or A-705253. (E) Aggregation of platelets from healthy and diabetic mice treated with vehicle or A-705253. The graphs summarize data obtained in platelets from 6-9 animals per group. *P < .05; **P < .01 versus CTL; #P < .05; ##P < .01 versus vehicle-treated diabetic mice.

Reversal of the diabetes-associated calpain overactivation by in vivo calpain inhibition. (A) ILK, septin-5, FAK, and PYK2 levels in platelets from healthy (CTL) and streptozotocin-induced diabetic mice (Dia) treated with vehicle or the calpain inhibitor A-705253 (A70). (B) CCL5 in microparticles isolated from the plasma of healthy (CTL) or diabetic (Dia) mice treated with vehicle or A-705253. (C) Effect of in vivo A-705253 treatment on thrombus size after FeCl3-induced injury of carotid arteries from healthy (top panel) and diabetic (bottom panel) mice. (D) Number of circulating platelet-leukocyte aggregates in healthy (CTL) and diabetic (Dia) mice treated with vehicle or A-705253. (E) Aggregation of platelets from healthy and diabetic mice treated with vehicle or A-705253. The graphs summarize data obtained in platelets from 6-9 animals per group. *P < .05; **P < .01 versus CTL; #P < .05; ##P < .01 versus vehicle-treated diabetic mice.

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