Plasma concentrations of sVEGFR-1 (A), PlGF (B), Ang2 (C), VEGF (D), and sTie2 (E) were measured in control subjects (n = 23) and patients with PAD (n = 46). Concentrations of sVEGFR-1 and PlGF were not significantly different between the 2 populations; however, Ang2 (*p < 0.0001), VEGF (*p < 0.01), and sTie2 (*p < 0.01) were significantly greater in PAD patients. Ang2 = angiopoietin-2; PAD = peripheral arterial disease; PlGF = placenta growth factor; sTie2 = soluble Tie2; sVEGFR = soluble vascular endothelial growth factor receptor; VEGF = vascular endothelial growth factor.

Plasma concentrations of Ang2, VEGF, and sTie2 were measured and compared in control subjects (n = 23) and patients with IC (n = 23) or CLI (n = 23). (A) Plasma concentrations of Ang2 were significantly increased in both IC (**p < 0.01) and CLI (***p < 0.0001) patients compared with control subjects, but there was no significant difference between IC and CLI. (B) Vascular endothelial growth factor levels were significantly increased in CLI patients compared with control subjects (**p < 0.01) and IC (*p < 0.05), but there was no difference between IC and control subjects. (C) sTie2 concentrations were significantly greater in CLI patients compared with control subjects (***p < 0.0001) and IC (***p < 0.0001), but there was no difference between IC and control subjects. CLI = critical limb ischemia; IC = intermittent claudication; other abbreviations as in Figure 1.

Human umbilical vein endothelial cells were stimulated with VEGF-A₁₆₅ (25 ng/ml) for 24 h. Concentration of sTie2 in the cell-conditioned medium was quantified by enzyme-linked immunoadsorbent assay. Vascular endothelial growth factor treatment significantly increased release of sTie2 (*p < 0.01). Abbreviations as in Figure 1.