@article {44,
	title = {VEGF-C/VEGFR-3 Signaling Regulates Inflammatory Response in Development of Obliterative Airway Disease},
	journal = {Journal of Heart and Lung Transplantation},
	volume = {30},
	year = {2011},
	month = {2011//},
	pages = {S118 - S118},
	author = {Krebs, R and Tikkanen, JM and Ropponen, JO and Jeltsch, M and Jokinen, JJ and Yl{\"a}-Herttuala, S and Koskinen, PK and Nyk{\"a}nen, AI and Lemstr{\"o}m, KB}
}
@article {23,
	title = {Vascular endothelial growth factor-C-mediated lymphangiogenesis promotes tumour metastasis},
	journal = {EMBO J},
	volume = {20},
	year = {2001},
	month = {2001/Feb/},
	pages = {672 - 82},
	abstract = {Metastasis is a frequent and lethal complication of cancer. Vascular endothelial growth factor-C (VEGF-C) is a recently described lymphangiogenic factor. Increased expression of VEGF-C in primary tumours correlates with dissemination of tumour cells to regional lymph nodes. However, a direct role for VEGF-C in tumour lymphangiogenesis and subsequent metastasis has yet to be demonstrated. Here we report the establishment of transgenic mice in which VEGF-C expression, driven by the rat insulin promoter (Rip), is targeted to beta-cells of the endocrine pancreas. In contrast to wild-type mice, which lack peri-insular lymphatics, RipVEGF-C transgenics develop an extensive network of lymphatics around the islets of Langerhans. These mice were crossed with Rip1Tag2 mice, which develop pancreatic beta-cell tumours that are neither lymphangiogenic nor metastatic. Double-transgenic mice formed tumours surrounded by well developed lymphatics, which frequently contained tumour cell masses of beta-cell origin. These mice frequently developed pancreatic lymph node metastases. Our findings demonstrate that VEGF-C-induced lymphangiogenesis mediates tumour cell dissemination and the formation of lymph node metastases.},
	url = {http://view.ncbi.nlm.nih.gov/pubmed/11179212},
	author = {Mandriota, S J and Jussila, L and Jeltsch, M and Compagni, A and Baetens, D and Prevo, R and Banerji, S and Huarte, J and Montesano, R and Jackson, D G and Orci, L and Alitalo, K and Christofori, G and Pepper, M S}
}
@article {16,
	title = {Vascular endothelial growth factor D (VEGF-D) is a ligand for the tyrosine kinases VEGF receptor 2 (Flk1) and VEGF receptor 3 (Flt4)},
	journal = {Proc Natl Acad Sci U S A},
	volume = {95},
	year = {1998},
	month = {1998/Jan/},
	pages = {548 - 53},
	abstract = {We have identified a member of the VEGF family by computer-based homology searching and have designated it VEGF-D. VEGF-D is most closely related to VEGF-C by virtue of the presence of N- and C-terminal extensions that are not found in other VEGF family members. In adult human tissues, VEGF-D mRNA is most abundant in heart, lung, skeletal muscle, colon, and small intestine. Analyses of VEGF-D receptor specificity revealed that VEGF-D is a ligand for both VEGF receptors (VEGFRs) VEGFR-2 (Flk1) and VEGFR-3 (Flt4) and can activate these receptors. However. VEGF-D does not bind to VEGFR-1. Expression of a truncated derivative of VEGF-D demonstrated that the receptor-binding capacities reside in the portion of the molecule that is most closely related in primary structure to other VEGF family members and that corresponds to the mature form of VEGF-C. In addition, VEGF-D is a mitogen for endothelial cells. The structural and functional similarities between VEGF-D and VEGF-C define a subfamily of the VEGFs.},
	url = {http://view.ncbi.nlm.nih.gov/pubmed/9435229},
	author = {Achen, M G and Jeltsch, M and Kukk, E and M{\"a}kinen, T and Vitali, A and Wilks, A F and Alitalo, K and Stacker, S A}
}
@article {15,
	title = {Vascular endothelial growth factor (VEGF)-C synergizes with basic fibroblast growth factor and VEGF in the induction of angiogenesis in vitro and alters endothelial cell extracellular proteolytic activity},
	journal = {J Cell Physiol},
	volume = {177},
	year = {1998},
	month = {1998/Dec/},
	pages = {439 - 52},
	abstract = {Vascular endothelial growth factor-C (VEGF-C) is a recently characterized member of the VEGF family of angiogenic polypeptides. We demonstrate here that VEGF-C is angiogenic in vitro when added to bovine aortic or lymphatic endothelial (BAE and BLE) cells but has little or no effect on bovine microvascular endothelial (BME) cells. As reported previously for VEGF, VEGF-C and basic fibroblast growth factor (bFGF) induced a synergistic in vitro angiogenic response in all three cells lines. Unexpectedly, VEGF and VEGF-C also synergized in the in vitro angiogenic response when assessed on BAE cells. Characterization of VEGF receptor (VEGFR) expression revealed that BME, BAE, and BLE cell lines express VEGFR-1 and -2, whereas of the three cell lines assessed, only BAE cells express VEGFR-3. We also demonstrate that VEGF-C increases plasminogen activator (PA) activity in the three bovine endothelial cell lines and that this is accompanied by a concomitant increase in PA inhibitor-1. Addition of alpha2-antiplasmin to BME cells co-treated with bFGF and VEGF-C partially inhibited collagen gel invasion. These results demonstrate, first, that by acting in concert with bFGF or VEGF, VEGF-C has a potent synergistic effect on the induction of angiogenesis in vitro and, second, that like VEGF and bFGF, VEGF-C is capable of altering endothelial cell extracellular proteolytic activity. These observations also highlight the notion of context, i.e., that the activity of an angiogenesis-regulating cytokine depends on the presence and concentration of other cytokines in the pericellular environment of the responding endothelial cell.},
	url = {http://view.ncbi.nlm.nih.gov/pubmed/9808152},
	author = {Pepper, M S and Mandriota, S J and Jeltsch, M and Kumar, V and Alitalo, K}
}
@article {12,
	title = {Vascular endothelial growth factors VEGF-B and VEGF-C},
	journal = {J Cell Physiol},
	volume = {173},
	year = {1997},
	month = {1997/Nov/},
	pages = {211 - 5},
	url = {http://view.ncbi.nlm.nih.gov/pubmed/9365524},
	author = {Joukov, V and Kaipainen, A and Jeltsch, M and Pajusola, K and Olofsson, B and Kumar, V and Eriksson, U and Alitalo, K}
}
@article {9,
	title = {VEGF-C receptor binding and pattern of expression with VEGFR-3 suggests a role in lymphatic vascular development},
	journal = {Development},
	volume = {122},
	year = {1996},
	month = {1996/Dec/},
	pages = {3829 - 37},
	abstract = {The vascular endothelial growth factor family has recently been expanded by the isolation of two new VEGF-related factors, VEGF-B and VEGF-C. The physiological functions of these factors are largely unknown. Here we report the cloning and characterization of mouse VEGF-C, which is produced as a disulfide-linked dimer of 415 amino acid residue polypeptides, sharing an 85\% identity with the human VEGF-C amino acid sequence. The recombinant mouse VEGF-C protein was secreted from transfected cells as VEGFR-3 (Flt4) binding polypeptides of 30-32x10(3) Mr and 22-23x10(3) Mr which preferentially stimulated the autophosphorylation of VEGFR-3 in comparison with VEGFR-2 (KDR). In in situ hybridization, mouse VEGF-C mRNA expression was detected in mesenchymal cells of postimplantation mouse embryos, particularly in the regions where the lymphatic vessels undergo sprouting from embryonic veins, such as the perimetanephric, axillary and jugular regions. In addition, the developing mesenterium, which is rich in lymphatic vessels, showed strong VEGF-C expression. VEGF-C was also highly expressed in adult mouse lung, heart and kidney, where VEGFR-3 was also prominent. The pattern of expression of VEGF-C in relation to its major receptor VEGFR-3 during the sprouting of the lymphatic endothelium in embryos suggests a paracrine mode of action and that one of the functions of VEGF-C may be in the regulation of angiogenesis of the lymphatic vasculature.},
	url = {http://view.ncbi.nlm.nih.gov/pubmed/9012504},
	author = {Kukk, E and Lymboussaki, A and Taira, S and Kaipainen, A and Jeltsch, M and Joukov, V and Alitalo, K}
}
