%0 Journal Article %1 Tammela.2008 %A Tammela, T. %A Zarkada, G. %A Wallgard, E. %A Murtomaki, A. %A Suchting, S. %A Wirzenius, M. %A Waltari, M. %A Hellstrom, M. %A Schomber, T. %A Peltonen, R. %A Freitas, C. %A Duarte, A. %A Isoniemi, H. %A Laakkonen, P. %A Christofori, G. %A Yla-Herttuala, S. %A Shibuya, M. %A Pytowski, B. %A Eichmann, A. %A Betsholtz, C. %A Alitalo, K. %D 2008 %J Nature %K & Adult Angiogenesis Animals Antibodies BALB Blood C Cell Cells Dipeptides Down-Regulation Endothelial Endothelium Expression Factor Factors Female Gene Growth Humans Inbred Inhibitors Laboratories Ligands Line Lymphangiogenesis Mice Monoclonal Neoplasms Neoplastic Neovascularization Notch Pathologic Proliferation Receptor-3 Receptors Regulation Research Signal Transduction Transgenic Tumor Tyrosine Vascular Vessels antagonists blood cells drug effects genetics inhibitors metabolism pharmacology supply therapy %N 7204 %P 656-660 %T Blocking VEGFR-3 suppresses angiogenic sprouting and vascular network formation %U PM:18594512 %V 454 %X Angiogenesis, the growth of new blood vessels from pre-existing vasculature, is a key process in several pathological conditions, including tumour growth and age-related macular degeneration. Vascular endothelial growth factors (VEGFs) stimulate angiogenesis and lymphangiogenesis by activating VEGF receptor (VEGFR) tyrosine kinases in endothelial cells. VEGFR-3 (also known as FLT-4) is present in all endothelia during development, and in the adult it becomes restricted to the lymphatic endothelium. However, VEGFR-3 is upregulated in the microvasculature of tumours and wounds. Here we demonstrate that VEGFR-3 is highly expressed in angiogenic sprouts, and genetic targeting of VEGFR-3 or blocking of VEGFR-3 signalling with monoclonal antibodies results in decreased sprouting, vascular density, vessel branching and endothelial cell proliferation in mouse angiogenesis models. Stimulation of VEGFR-3 augmented VEGF-induced angiogenesis and sustained angiogenesis even in the presence of VEGFR

@article{Tammela.2008, abstract = {Angiogenesis, the growth of new blood vessels from pre-existing vasculature, is a key process in several pathological conditions, including tumour growth and age-related macular degeneration. Vascular endothelial growth factors (VEGFs) stimulate angiogenesis and lymphangiogenesis by activating VEGF receptor (VEGFR) tyrosine kinases in endothelial cells. VEGFR-3 (also known as FLT-4) is present in all endothelia during development, and in the adult it becomes restricted to the lymphatic endothelium. However, VEGFR-3 is upregulated in the microvasculature of tumours and wounds. Here we demonstrate that VEGFR-3 is highly expressed in angiogenic sprouts, and genetic targeting of VEGFR-3 or blocking of VEGFR-3 signalling with monoclonal antibodies results in decreased sprouting, vascular density, vessel branching and endothelial cell proliferation in mouse angiogenesis models. Stimulation of VEGFR-3 augmented VEGF-induced angiogenesis and sustained angiogenesis even in the presence of VEGFR}, added-at = {2010-02-05T11:28:39.000+0100}, author = {Tammela, T. and Zarkada, G. and Wallgard, E. and Murtomaki, A. and Suchting, S. and Wirzenius, M. and Waltari, M. and Hellstrom, M. and Schomber, T. and Peltonen, R. and Freitas, C. and Duarte, A. and Isoniemi, H. and Laakkonen, P. and Christofori, G. and Yla-Herttuala, S. and Shibuya, M. and Pytowski, B. and Eichmann, A. and Betsholtz, C. and Alitalo, K.}, biburl = {https://www.bibsonomy.org/bibtex/2b27000713c04489b8399bb1ffbbb30d3/kanefendt}, interhash = {0075498eb4228e559581212491ea84f0}, intrahash = {b27000713c04489b8399bb1ffbbb30d3}, journal = {Nature}, keywords = {& Adult Angiogenesis Animals Antibodies BALB Blood C Cell Cells Dipeptides Down-Regulation Endothelial Endothelium Expression Factor Factors Female Gene Growth Humans Inbred Inhibitors Laboratories Ligands Line Lymphangiogenesis Mice Monoclonal Neoplasms Neoplastic Neovascularization Notch Pathologic Proliferation Receptor-3 Receptors Regulation Research Signal Transduction Transgenic Tumor Tyrosine Vascular Vessels antagonists blood cells drug effects genetics inhibitors metabolism pharmacology supply therapy}, number = 7204, pages = {656-660}, timestamp = {2010-02-05T11:28:50.000+0100}, title = {Blocking VEGFR-3 suppresses angiogenic sprouting and vascular network formation}, url = {PM:18594512}, volume = 454, year = 2008 }