Figure 2.

The ferroptosis-like mechanism driven by Erastin (Era) promotes endothelial cell (ECs) activation and Propranolol (Prop) impairs the phenotype induced by Era exposure. (A) The ferroptosis-like mechanism, generated by Era exposure, promotes HUVECs proliferation (increased ratio of Ki67⁺ (green) nuclei/total nuclei), while Prop decreases the rate of HUVECs proliferation and impairs the phenotype induced by Era. The panel shows representative microscope images of the Ki67 staining. (B) Era fosters HUVECs migration (increased % wound closure) and Prop inhibits and reverts the phenotype induced by Era. (C, D) Era increases the branch point density of vessel-like structures (proxy for vascular density) at the same range of H₂O₂ (ROS; positive control), with no additive effect. Prop, besides the impairment of vessel-like structures formation (decreased branch point density), inhibits the phenotype induced by Era, even when Prop is added to the vessel-like structures already formed in the presence of Era (Era+Prop (2h)) and contrariwise (Prop+Era (2h)). In graphs the dashed line represents the control condition. All data are normalized to the control condition and represented as mean ± SD. **p<0.01, ***p<0.001, ****p<0.0001.