@article {24,
	title = {Adenoviral VEGF-C overexpression induces blood vessel enlargement, tortuosity, and leakiness but no sprouting angiogenesis in the skin or mucous membranes},
	journal = {FASEB J},
	volume = {16},
	year = {2002},
	month = {2002/Jul/},
	pages = {1041 - 9},
	abstract = {Vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs) are important regulators of blood and lymphatic vessel growth and vascular permeability. The VEGF-C/VEGFR-3 signaling pathway is crucial for lymphangiogenesis, and heterozygous inactivating missense mutations of the VEGFR-3 gene are associated with hereditary lymphedema. However, VEGF-C can have potent effects on blood vessels because its receptor VEGFR-3 is expressed in certain blood vessels and because the fully processed form of VEGF-C also binds to the VEGFR-2 of blood vessels. To characterize the in vivo effects of VEGF-C on blood and lymphatic vessels, we have overexpressed VEGF-C via adenovirus- and adeno-associated virus-mediated transfection in the skin and respiratory tract of athymic nude mice. This resulted in dose-dependent enlargement and tortuosity of veins, which, along with the collecting lymphatic vessels were found to express VEGFR-2. Expression of angiopoietin 1 blocked the increased leakiness of the blood vessels induced by VEGF-C whereas vessel enlargement and lymphangiogenesis were not affected. However, angiogenic sprouting of new blood vessels was not observed in response to AdVEGF-C or AAV-VEGF-C. These results show that virally produced VEGF-C induces blood vessel changes, including vascular leak, but its angiogenic potency is much reduced compared with VEGF in normal skin.},
	url = {http://view.ncbi.nlm.nih.gov/pubmed/12087065},
	author = {Saaristo, Anne and Veikkola, Tanja and Enholm, Berndt and Hyt{\"o}nen, Maija and Arola, Johanna and Pajusola, Katri and Turunen, Pa{\"\i}vi and Jeltsch, Michael and Karkkainen, Marika J and Kerjaschki, Dontscho and Bueler, Hansruedi and Yl{\"a}-Herttuala, Seppo and Alitalo, Kari}
}
