Erratum to: Annals of Biomedical Engineering DOI 10.1007/s10439-015-1442-0

The original publication of the article contained errors owing to selecting inappropriate images as representative of different experimental groups when processing and assembling figures in Figs. 2c and 4b. The corrected Figs. 2c and 4b are given below. The authors sincerely apologize for these errors.

Figure 2
figure 2

Inhibition of AAMP impairs VEGF-induced angiogenesis. (a) Immuno-blot analysis of AAMP expression in HUVECs transfected with siRNAs expressing vetor si-AAMP-1 and si-AAMP-2 that targeting AAMP or control siRNA expressing vetor si-con. (b) Quantitative analysis of AAMP protein expression (**p < 0.01 vs. none transfected cells). (c) HUVECs transfected with si-AAMP or si-con were plated onto matrigel, and photographs were taken 16 h later. (d) Aortic ring sprouting angiogenesis impaired by anti-AAMP antibody. (e) Quantitative analysis of relative tube length on matrigel. (*p < 0.05 vs. transfected with si-con and without VEGF stimulation, **p < 0.01 vs. si-con and without VEGF stimulation, ## p < 0.01 vs. transfected with si-con and VEGF stimulation. (f) Quantitative analysis of the number of the microvessels sprouting from aortic ring. (**p < 0.01 vs. no anti-serum treatment).

Figure 4
figure 4

AAMP modulates angiogenesis by mediating cell migration and spreading. (a) HUVECs transfected with si-con, si-AAMP-1 and si-AAMP-2 plasmids were scratched, and wound margins were imaged 16 h later. (b) HUVECs transfected with si-con and si-AAMP-1 or si-AAMP-2 plasmids were plated onto Matrigel, and photographs were taken 60 min later. (c) The extent of wound closure was quantified by measuring the wound area compared with the initial wound area (**p < 0.01 vs. si-con). (d) The degree of cell spreading was quantified with cell area 60 min after plating (**p < 0.01 vs. si-con).