Effect of VEGF in α2-AP^+/+ mice and of α2-AP in α2-AP^-/- mice. Scanning electron photomicrographs of the regenerated endothelial surface of a carotid artery 48 hours after injury in α2-AP^+/+ mice treated with VEGF at a dose of 8 ng per body (A) and treated with α2-AP at a dose of 75 mg per body (C). Cell proliferation (n = 4) measured as the BrdU index (percentage) of recovered endothelial cell layer (□) and SMCs in media (•) following vascular injury in α2-AP^+/+ mice (B). VEGF (2, 4, 8 ng/body) was injected as a bolus before the initiation of endothelial injury. BrdU (50 mg/kg) was injected subcutaneously 1, 8, 16, and 24 hours prior to removal of the carotid arteries. Two days after the injury, the injured artery was removed and stained for the measurement of BrdU-positive cells. The development of neointima in α2-AP^-/- mice is shown as the percentage of luminal stenosis by newly formed intima (D). α2-AP was injected as a bolus via tail vein for 1 day, 3 days, 1 week, 2 weeks, or 4 weeks after endothelial injury, and the injured carotid artery was removed 4 weeks after injury (n = 4 each). α2-AP^+/+ mice (wild type [WT]) were treated with α2-AP for 4 weeks. ^* indicates P < .05 versus control (without α2-AP). Scale bar represents 10 μm.