Fig. 9
From: NCK-dependent pericyte migration promotes pathological neovascularization in ischemic retinopathy
Model for pericyte NCK1/2 function in vascular development and ischemic retinopathy. During angiogenic sprouting, tip cells express PDGF-B to recruit the pericytes and stabilize the new vessels. PDGFRβ activation on the surface of pericytes leads to NCK1/2-dependent PAK activation and pericyte migration. Under ischemic conditions, high PDGF-B levels activate pericyte α-SMA expression and increase vessel coverage, including tip cells. Dysfunctional α-SMA+ pericytes promote pathological angiogenesis and inhibit retinal revascularization. Inhibition of PDGF-B or PDGFRβ downstream NCK1/2 signaling blocks pericyte recruitment and NVTs and promotes vessel regrowth in the OIR retina
