Figure 4. SCP1 inhibited AKT-mediated angiogenesis.
(A) SCP1 deletion promoted VEGF-induced AKT activation in HUVECs. HUVECs were transfected with siNC (Small Interfering RNA for Normal Control) or siSCP1 (Small Interfering RNA for SCP1) for 72 h and stimulated with VEGF (100 ng/ml) as indicated after starvation for 8 h. (B) SCP1 impaired HUVEC tube formation through AKT. HUVECs were overexpressed with SCP1 with or without AKT-S473D. The cells were placed in plates coated with Matrigel and tubular structures were photographed after 6 h. The tube lengths were measured in each field. *p<0.05. (C) SCP1 depletion inhibited the tube formation of HUVECs through AKT. HUVECs were transfected with siSCP1 and treated with or without AKT inhibitor (AKTi; MK2206, 2 nM) for 5 days as indicated. The tube lengths were measured in each field. **p<0.01, *p<0.05. (D) SCP1 deletion promoted HUVEC migration through AKT. Cell migration was detected using a wound healing assay. HUVECs were transfected and treated with or without AKTi (MK2206, 2 nM). The migration cell number in each field was calculated. **p<0.01, *p<0.05.
DOI: http://dx.doi.org/10.7554/eLife.22058.010
Figure 4—figure supplement 1. SCP1 inhibits HUVEC migration.
