@article {708,
	title = {VEGF-C Protects the Integrity of Bone Marrow Perivascular Niche},
	journal = {Blood},
	year = {2020},
	month = {2020/07/31/},
	pages = {accepted - for publication},
	abstract = {Key Points. Vegfc deletion in endothelial or LepR+ cells compromises the bone marrow perivascular niche and hematopoietic stem cell maintenance.Exogenous admin},
	doi = {10.1182/blood.2020005699},
	url = {https://ashpublications.org/blood/article/doi/10.1182/blood.2020005699/463465/VEGF-C-Protects-the-Integrity-of-Bone-Marrow}
}
@article {43,
	title = {Vascular endothelial growth factor-B acts as a coronary growth factor in transgenic rats without inducing angiogenesis, vascular leak, or inflammation},
	journal = {Circulation},
	volume = {122},
	year = {2010},
	month = {2010/Oct/},
	pages = {1725 - 33},
	abstract = {BACKGROUND: Vascular endothelial growth factor-B (VEGF-B) binds to VEGF receptor-1 and neuropilin-1 and is abundantly expressed in the heart, skeletal muscle, and brown fat. The biological function of VEGF-B is incompletely understood. METHODS AND RESULTS: Unlike placenta growth factor, which binds to the same receptors, adeno-associated viral delivery of VEGF-B to mouse skeletal or heart muscle induced very little angiogenesis, vascular permeability, or inflammation. As previously reported for the VEGF-B(167) isoform, transgenic mice and rats expressing both isoforms of VEGF-B in the myocardium developed cardiac hypertrophy yet maintained systolic function. Deletion of the VEGF receptor-1 tyrosine kinase domain or the arterial endothelial Bmx tyrosine kinase inhibited hypertrophy, whereas loss of VEGF-B interaction with neuropilin-1 had no effect. Surprisingly, in rats, the heart-specific VEGF-B transgene induced impressive growth of the epicardial coronary vessels and their branches, with large arteries also seen deep inside the subendocardial myocardium. However, VEGF-B, unlike other VEGF family members, did not induce significant capillary angiogenesis, increased permeability, or inflammatory cell recruitment. CONCLUSIONS: VEGF-B appears to be a coronary growth factor in rats but not in mice. The signals for the VEGF-B-induced cardiac hypertrophy are mediated at least in part via the endothelium. Because cardiomyocyte damage in myocardial ischemia begins in the subendocardial myocardium, the VEGF-B-induced increased arterial supply to this area could have therapeutic potential in ischemic heart disease.},
	url = {http://view.ncbi.nlm.nih.gov/pubmed/20937974},
	author = {Bry, Maija and Kivel{\"a}, Riikka and Holopainen, Tanja and Anisimov, Andrey and Tammela, Tuomas and Soronen, Jarkko and Silvola, Johanna and Saraste, Antti and Jeltsch, Michael and Korpisalo, Petra and Carmeliet, Peter and Lemstr{\"o}m, Karl B and Shibuya, Masabumi and Yl{\"a}-Herttuala, Seppo and Alhonen, Leena and Mervaala, Eero and Andersson, Leif C and Knuuti, Juhani and Alitalo, Kari}
}
@article {32,
	title = {Vascular endothelial growth factor (VEGF)/VEGF-C mosaic molecules reveal specificity determinants and feature novel receptor binding patterns},
	journal = {J Biol Chem},
	volume = {281},
	year = {2006},
	month = {2006/Apr/},
	pages = {12187 - 95},
	abstract = {Vascular endothelial growth factors (VEGFs) and their receptors play key roles in angiogenesis and lymphangiogenesis. VEGF activates VEGF receptor-1 (VEGFR-1) and VEGFR-2, whereas VEGF-C activates VEGFR-2 and VEGFR-3. We have created a library of VEGF/VEGF-C mosaic molecules that contains factors with novel receptor binding profiles, notably proteins binding to all three VEGF receptors ("super-VEGFs"). The analyzed super-VEGFs show both angiogenic and lymphangiogenic effects in vivo, although weaker than the parental molecules. The composition of the VEGFR-3 binding molecules and scanning mutagenesis revealed determinants of receptor binding and specificity. VEGFR-2 and VEGFR-3 showed striking differences in their requirements for VEGF-C binding; extracellular domain 2 of VEGFR-2 was sufficient, whereas in VEGFR-3, both domains 1 and 2 were necessary.},
	url = {http://view.ncbi.nlm.nih.gov/pubmed/16505489},
	author = {Jeltsch, Michael and Karpanen, Terhi and Strandin, Tomas and Aho, Kukka and Lankinen, Hilkka and Alitalo, Kari}
}
@inbook {480,
	title = {VEGF Receptors},
	booktitle = {Sigma-RBI Handbook of Receptor Classification and Signal Transduction},
	year = {2006},
	publisher = {Sigma},
	organization = {Sigma},
	edition = {5.},
	url = {http://www.sigmaaldrich.com/technical-documents/articles/biology/rbi-handbook.html}
}
@article {30,
	title = {Vascular endothelial cell growth factor receptor 3-mediated activation of lymphatic endothelium is crucial for tumor cell entry and spread via lymphatic vessels},
	journal = {Cancer Res},
	volume = {65},
	year = {2005},
	month = {2005/Jun/},
	pages = {4739 - 46},
	abstract = {Lymphangiogenic growth factors vascular endothelial growth factor (VEGF)-C and VEGF-D have been shown to promote lymphatic metastasis by inducing tumor-associated lymphangiogenesis. In this study, we have investigated how tumor cells gain access into lymphatic vessels and at what stage tumor cells initiate metastasis. We show that VEGF-C produced by tumor cells induced extensive lymphatic sprouting towards the tumor cells as well as dilation of the draining lymphatic vessels, suggesting an active role of lymphatic endothelial cells in lymphatic metastasis. A significant increase in lymphatic vessel growth occurred between 2 and 3 weeks after tumor xenotransplantation, and lymph node metastasis occurred at the same stage. These processes were blocked dose-dependently by inhibition of VEGF receptor 3 (VEGFR-3) signaling by systemic delivery of a soluble VEGFR-3-immunoglobulin (Ig) fusion protein via adenoviral or adeno-associated viral vectors. However, VEGFR-3-Ig did not suppress lymph node metastasis when the treatment was started at a later stage after the tumor cells had already spread out, suggesting that tumor cell entry into lymphatic vessels is a key step during tumor dissemination via the lymphatics. Whereas lymphangiogenesis and lymph node metastasis were significantly inhibited by VEGFR-3-Ig, some tumor cells were still detected in the lymph nodes in some of the treated mice. This indicates that complete blockade of lymphatic metastasis may require the targeting of both tumor lymphangiogenesis and tumor cell invasion.},
	url = {http://view.ncbi.nlm.nih.gov/pubmed/15930292},
	author = {He, Yulong and Rajantie, Iiro and Pajusola, Katri and Jeltsch, Michael and Holopainen, Tanja and Yla-Herttuala, Seppo and Harding, Thomas and Jooss, Karin and Takahashi, Takashi and Alitalo, Kari}
}
@article {28,
	title = {Vascular endothelial growth factor C is required for sprouting of the first lymphatic vessels from embryonic veins},
	journal = {Nat Immunol},
	volume = {5},
	year = {2004},
	month = {2004/Jan/},
	pages = {74 - 80},
	abstract = {Lymphatic vessels are essential for immune surveillance, tissue fluid homeostasis and fat absorption. Defects in lymphatic vessel formation or function cause lymphedema. Here we show that the vascular endothelial growth factor C (VEGF-C) is required for the initial steps in lymphatic development. In Vegfc-/- mice, endothelial cells commit to the lymphatic lineage but do not sprout to form lymph vessels. Sprouting was rescued by VEGF-C and VEGF-D but not by VEGF, indicating VEGF receptor 3 specificity. The lack of lymphatic vessels resulted in prenatal death due to fluid accumulation in tissues, and Vegfc+/- mice developed cutaneous lymphatic hypoplasia and lymphedema. Our results indicate that VEGF-C is the paracrine factor essential for lymphangiogenesis, and show that both Vegfc alleles are required for normal lymphatic development.},
	url = {http://view.ncbi.nlm.nih.gov/pubmed/14634646},
	author = {Karkkainen, Marika J and Haiko, Paula and Sainio, Kirsi and Partanen, Juha and Taipale, Jussi and Petrova, Tatiana V and Jeltsch, Michael and Jackson, David G and Talikka, Marja and Rauvala, Heikki and Betsholtz, Christer and Alitalo, Kari}
}
@article {26,
	title = {VEGF guides angiogenic sprouting utilizing endothelial tip cell filopodia},
	journal = {J Cell Biol},
	volume = {161},
	year = {2003},
	month = {2003/Jun/},
	pages = {1163 - 77},
	abstract = {Vascular endothelial growth factor (VEGF-A) is a major regulator of blood vessel formation and function. It controls several processes in endothelial cells, such as proliferation, survival, and migration, but it is not known how these are coordinately regulated to result in more complex morphogenetic events, such as tubular sprouting, fusion, and network formation. We show here that VEGF-A controls angiogenic sprouting in the early postnatal retina by guiding filopodial extension from specialized endothelial cells situated at the tips of the vascular sprouts. The tip cells respond to VEGF-A only by guided migration; the proliferative response to VEGF-A occurs in the sprout stalks. These two cellular responses are both mediated by agonistic activity of VEGF-A on VEGF receptor 2. Whereas tip cell migration depends on a gradient of VEGF-A, proliferation is regulated by its concentration. Thus, vessel patterning during retinal angiogenesis depends on the balance between two different qualities of the extracellular VEGF-A distribution, which regulate distinct cellular responses in defined populations of endothelial cells.},
	url = {http://view.ncbi.nlm.nih.gov/pubmed/12810700},
	author = {Gerhardt, Holger and Golding, Matthew and Fruttiger, Marcus and Ruhrberg, Christiana and Lundkvist, Andrea and Abramsson, Alexandra and Jeltsch, Michael and Mitchell, Christopher and Alitalo, Kari and Shima, David and Betsholtz, Christer}
}
