Fig. 3.

Involvement of Angiopoietins during vascular regression. a Vascular regression occurs under both, pathological and physiological settings and is characterized by local pericyte loss (turquois) and the disappearance of endothelial cells, leaving an empty basement membrane sleeve (“ghost vessels”/blue). b During vascular homeostasis shear stress is inducing Kruppel-like factor 2 (KLF2), a negative regulator of Angiopoietin-2 (Ang-2). Furthermore, Ang-1 (black) is secreted by mural cells into the extra cellular matrix (ECM/blue) and can then bind to endothelial expressed Tie2 (green) that will translocate to the cell–cell junctions upon Ang-1 binding forming homodimers in trans. Tie2 signaling further up-regulates KLF2 and stabilizes junctional molecules such as VE-cadherin (yellow). During vascular regression the occlusion of vessels leads to disturbed and reduced blood flow leading to KLF2 down-regulation. Ang-2 (orange) in turn becomes upregulated and triggers the dissociation of pericytes, the degradation of the basement membrane by inducing matrix metalloproteases (MMPs) and interferes with endothelial cell integrity