The FASEB Journal · 2007 · 118 citations · 45 references
Vegf Receptor-2Critical StepAngiogenesisAngiogenic Receptor Vegfr‐2Vascular Endothelial Growth FactorImmunologyPathologyMature Vegf-dVascular BiologyNeovascularizationSystems BiologyMedicineCell BiologyCell SignalingVegf-d ProcessingTumor Biology
Vascular endothelial growth factor (VEGF)-D is a secreted glycoprotein that induces angiogenesis and lymphangiogenesis. It consists of a central domain, containing binding sites for VEGF receptor-2 (VEGFR-2) and VEGFR-3, and N- and C-terminal propeptides. It is secreted from the cell as homodimers of the full-length form that can be proteolytically processed to remove the propeptides. It was recently shown, using adenoviral gene delivery, that fully processed VEGF-D induces angiogenesis in vivo, whereas full-length VEGF-D does not. To better understand these observations, we monitored the effect of VEGF-D processing on receptor binding using a full-length VEGF-D mutant that cannot be processed. This mutant binds VEGFR-2, the receptor signaling for angiogenesis, with approximately 17,000-fold lower affinity than mature VEGF-D, indicating the importance of processing for interaction with this receptor. Further, we show that members of the proprotein convertase (PC) family of proteases promote VEGF-D processing, which facilitates the VEGF-D/VEGFR-2 interaction. The PCs furin and PC5 promote cleavage of both propeptides, whereas PC7 promotes cleavage of the C-terminal propeptide only. The finding that PCs promote activation of VEGF-D and other proteins with roles in cancer such as matrix metalloproteinases, emphasizes the importance of these enzymes as potential regulators of tumor progression and metastasis.
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VEGF-D promotes the metastatic spread of tumor cells via the lymphatics
Steven A. Stacker, Carol Caesar, Megan E. Baldwin et al. · Nature Medicine · 2001 · 1.2K citations