VEGF-mediated signal transduction in lymphatic endothelial cells |
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| Authors: | Fuad Bahram Lena Claesson-Welsh |
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| Institution: | 1. Gastroenterology Department, Hotel Dieu de France University Hospital, Beirut, Lebanon;2. Radiology Department, Hotel Dieu de France University Hospital, Beirut, Lebanon;3. Surgery Department, Hotel Dieu de France University Hospital, Beirut, Lebanon;1. Department of Obstetrics and Gynecology, Guangdong Women and Children Hospital, Guangzhou, Guangdong 511400, People''s Republic of China;2. Department of Urology, The First Affiliated Hospital, Jinan University, Huangpu Avenue West 601, Guangzhou, Guangdong 510630, People''s Republic of China;3. Department of Pathology, Guangdong Women and Children Hospital, Guangzhou, Guangdong 511400, People''s Republic of China;1. Division of Cardiovascular Medicine, Stanford University, Stanford, CA, USA;2. Center for Tissue Regeneration, Repair and Restoration, Veterans Affairs Palo Alto Health Care System, 3801 Miranda Avenue, Palo Alto, CA 94304, USA;3. The Cardiovascular Institute, Stanford, CA, USA;4. Fibralign Corp, Sunnyvale, CA, USA;5. Department of Chemical Engineering, Stanford University, Stanford, CA, USA;1. MediCity Research Laboratory and Institute of Biomedicine, University of Turku, Turku, Finland;2. Laboratory of Immunology and Vascular Biology, Department of Pathology, School of Medicine, Stanford University, Stanford, CA, USA;3. Veterans Affairs Palo Alto Health Care System and The Palo Alto Veterans Institute for Research, Palo Alto, CA, USA;4. Turku Centre for Biotechnology, University of Turku, Turku, Finland;5. Department of Pathology, Turku University Hospital, Turku, Finland;6. Department of Plastic and General Surgery, Turku University Hospital, Turku, Finland;7. Department of Otorhinolaryngology, Turku University Hospital and University of Turku, Finland;8. Interdisciplinary Program for Biomedical Sciences, Institute for Academic Initiatives, Osaka University, Suita, Japan |
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| Abstract: | The VEGF family of angiogenic ligands consists of VEGFA, VEGFB, VEGFC, VEGFD and placenta growth factor, PlGF. These growth factors bind in an overlapping pattern to three receptor tyrosine kinases, denoted VEGFR1, VEGFR2 and VEGFR3. Originally, VEGFA (the prototype VEGF) was described as a master regulator of vascular endothelial cell biology in vitro and in vivo, transducing its effect through VEGFR2. VEGFA, VEGFB and PlGF bind to VEGFR1, which is a negative regulator of endothelial cell function at least during embryogenesis. VEGFC and VEGFD were identified as lymphatic endothelial factors, acting via VEGFR3. With time, the very clear distinction between the roles of the VEGF ligands in angiogenesis/lymphangiogenesis has given way for a more complex pattern. It seems that the biology of the different VEGFR2 and VEGFR3 ligands overlaps quite extensively and that both receptor types contribute to angiogenesis as well as lymphangiogenesis. This paradigm shift in our understanding is due to the access to more sophisticated reagents and techniques revealing dynamic and plastic expression of ligands and receptors in different physiological and pathological conditions. Moreover, knowledge on the important role of VEGF coreceptors, the neuropilins, in regulating the responsiveness to VEGF has changed our perception on the mechanism of VEGF signal transduction. This review will primarily focus on the properties of VEGR3, its signal transduction and the resulting biology. |
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