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Involvement of VEGFR-2 (kdr/flk-1) but not VEGFR-1 (flt-1) in VEGF-A and VEGF-C-induced tube formation by human microvascular endothelial cells in fibrin matrices in vitro Koolwijk P; Peters E; van der Vecht B; Hornig C; Weich HA; Alitalo K; Hicklin DJ; Wu Y; Witte L; van Hinsbergh VWAngiogenesis 2001[]; 4 (1): 53-60Different forms of vascular endothelial growth factor (VEGF) and their cellular receptors (VEGFR) are associated with angiogenesis, as demonstrated by the lethality of VEGF-A, VEGFR-1 or VEGFR-2 knockout mice. Here we have used an in vitro angiogenesis model, consisting of human microvascular endothelial cells (hMVEC) cultured on three-dimensional (3D) fibrin matrices to investigate the roles of VEGFR-1 and VEGFR-2 in the process of VEGF-A and VEGF-C-induced tube formation. Soluble VEGFR-1 completely inhibited the tube formation induced by the combination of VEGF-A and TNF alpha (VEGF-A/TNF alpha). This inhibition was not observed when tube formation was induced by VEGF-C/TNF alpha or bFGF/TNF alpha. Blocking monoclonal antibodies specific for VEGFR-2, but not antibodies specifically blocking VEGFR-1, were able to inhibit the VEGF-A/TNF alpha-induced as well as the VEGF-C/TNF alpha-induced tube formation in vitro. P1GF-2, which interacts only with VEGFR-1, neither induced tube formation in combination with TNF alpha, nor inhibited or stimulated by itself the VEGF-A/TNF alpha-induced tube formation in vitro. These data indicate that VEGF-A or VEGF-C activation of the VEGFR-2, and not of VEGFR-1, is involved in the formation of capillary-like tubular structures of hMVEC in 3D fibrin matrices used as a model of repair-associated or pathological angiogenesis in vitro.|Animals[MESH]|Antibodies, Monoclonal/pharmacology[MESH]|Cells, Cultured[MESH]|Endothelial Growth Factors/*pharmacology[MESH]|Endothelium, Vascular/*drug effects/*growth & development/physiology[MESH]|Humans[MESH]|In Vitro Techniques[MESH]|Mice[MESH]|Models, Cardiovascular[MESH]|Neovascularization, Physiologic/*drug effects[MESH]|Proto-Oncogene Proteins/antagonists & inhibitors/*physiology[MESH]|Receptor Protein-Tyrosine Kinases/antagonists & inhibitors/*physiology[MESH]|Receptors, Growth Factor/antagonists & inhibitors/*physiology[MESH]|Receptors, Vascular Endothelial Growth Factor[MESH]|Vascular Endothelial Growth Factor A[MESH]|Vascular Endothelial Growth Factor C[MESH]|Vascular Endothelial Growth Factor Receptor-1[MESH] |