Figure 7.

Schematic representation of the two-step mechanism employed by endothelial cells (ECs) to activate Erk-signalling following vessel wounding. Pre-ablation (left), the majority of ECs are Erk-signalling inactive. Following vessel wounding (middle), both ablated and adjacent intersegmental vessel (ISV) ECs rapidly activate Erk-signalling. Ca²⁺ signalling is also rapidly activated following vessel wounding but only in ablated ISV ECs, particularly in ECs close to the wounded site. Ca²⁺ signalling activity contributes to the activation of Erk-signalling in ablated ISV ECs in a sequential manner, starting from ECs close to the wounded site. Erk-signalling in adjacent ISV ECs has returned to pre-wound levels by 3 hours post-ablation (hpa) (right). Erk activity in ablated vessel ISV ECs is sustained through Vegfr-signalling. ECs closer to the wounded site are less sensitive to Vegfr-signalling inhibition, with higher signalling compared to ECs farther away. Recruited macrophages are essential for vessel regeneration but not the sole source of Vegfs at 3 hpa.