@mastersthesis {71,
	title = {Functional Analysis of VEGF-B and VEGF-C},
	volume = {Master{\textquoteright}s Thesis},
	year = {1997},
	school = {Univeristy of Helsinki},
	type = {M.Sc.},
	address = {Helsinki},
	abstract = {Vascular endothelial growth factor (VEGF) is an important regulator of endothelial cell proliferation and migration dur-
ing embryonic vasculogenesis and angiogenesis as well as in pathological angiogenesis. The recently cloned new factors
structurally homologous to VEGF were designated as VEGF-B/VRF and VEGF-C/VRP. The receptor for VEGF-B is
unknown. VEGF-C is the ligand for FLT4, a receptor tyrosine kinase whose expression becomes restricted largely to
lymphatic endothelia during development and that is related to VEGF receptors FLT1 and KDR.
In this study keratin 14-promoter-directed VEGF-C overexpression in the basal epidermis of transgenic mice was capa-
ble of promoting an abundant growth of extensive lymphatic-like vessel structures in the dermis, including large vessel
lacunae resembling in their histopathology the human condition known as lymphangioma. Thus, VEGF-C appears to
induce selective angiogenesis of the lymphatic vessels in vivo. In contrast, preliminary data on mice, which overexpress
VEGF-B under the same promoter, does not yet allow us draw any conclusions about its possible biological function.
Recombinant biologically active human VEGF-C was produced using the baculovirus system. Unpurified and purified
VEGF-C were used to confirm the interaction of VEGF-C with KDR, a fact recently missed by others. The recombinant
protein is going to be used in a large number of future experiments. The production of VEGF-B seems to be intrinsically
difficult in non-mammalian cells. Although quantitatively satisfying results could not be obtained yet, the purified
growth factor will be used in experiments to identify its receptor.},
	keywords = {VEGF-B, VEGF-C},
	url = {http://urn.fi/URN:NBN:fi-fe977347},
	author = {Jeltsch, Michael}
}
