Hydrogen peroxide inhibits HUVEC migration, whereas it increases APC migratory activity. (A) HUVEC monolayers were scratched and stimulated with vascular endothelial growth factor (VEGF) (100 ng/ml) in the presence or absence of H2O2 (250 μM). Phase-contrast images were collected after 24 h. H2O2 delayed HUVEC migration under basal conditions or VEGF stimulation. (B) Histograms indicating the percentage of gap closure: Values are means±SEM of three independent experiments, *p<0.05 versus untreated cells; #p<0.005 versus VEGF-treated cells. (C) SVEC monolayers were scratched and subjected to the same stimuli of HUVEC. (D) Histograms indicating the percentage of gap closure: Values are means±SEM of three independent experiments, *p<0.05 versus untreated cells; #p<0.005 versus VEGF-treated cells. (E) APC monolayers were scratched and incubated with PDGF (100 ng/ml) or SU6656 (5 μM) in the presence or absence of H2O2 (250 μM). H2O2 increased the unstimulated APC migration while leaving unmodified the pro-migratory effect of PDGF. Src inhibition by SU6656 inhibits the H2O2-induced migration of APCs, without affecting untreated cells. (F) Histograms illustrating the percentage of gap closure: Values are means±SEM of three independent experiments, *p<0.05 versus untreated cells. #p<0.005 versus H2O2 treated cells.