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. 2020 Mar 24;8:183. doi: 10.3389/fcell.2020.00183

FIGURE 4.

FIGURE 4

Molecular control of renal endothelial migration and patterning. VEGF is secreted by UB and NPC cells. Binding of VEGF to its tyrosine kinase receptor (KDR) activates three major signaling pathways: RAS/MAPK, DAG/PKC/MAPK, and PI3-K/AKT. Thus, it stimulates mitotic proliferation, survival, and migration of endothelial cells and promotes vascular network formation. UB cells produce SCF and induce survival, migration, and tube formation of endothelial cells. Expressions of WNT7b and WNT9b in the medullary ureteric epithelium regulate capillary lumen formation through modulation of VE-cadherin localization. AKT, protein kinase B; APC, adenomatous polyposis coli; c-Kit, tyrosine-protein kinase KIT (CD117); CK1, casein kinase 1; DAG, diacylglycerol; EC, endothelial cells; ERK, extracellular signal-regulated kinase; FRS2α, fibroblast growth factor receptor substrate 2; Frz, Frizzled; GAB1, Grb2-associated binder 1; GSK-3β, glycogen synthase kinase 3β; GRB2, growth factor receptor-bound protein 2; KDR, kinase insert domain protein receptor; MAPK, mitogen activated protein kinase; MEK, mitogen activated protein kinase; P, phosphate group; PI3K, phosphatidylinositol 3-kinase; PKC, protein kinase C; PLC-γ, phospholipase C-γ; RAS/RAF, Rat sarcoma/rapidly accelerated fibrosarcoma; SCF, stem cell factor; SOS, Son of Sevenless; VEGF, vascular endothelial growth factor; WNT, wingless-type mouse mammary tumor virus integration site.