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Gene Review

Vegfc  -  vascular endothelial growth factor C

Rattus norvegicus

Synonyms: Flt4 ligand, Flt4-L, VEGF-C, VRP, Vascular endothelial growth factor C, ...
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Disease relevance of Vegfc

  • Secondly, ectopic expression in the weakly metastatic NM-081 cell line of a mutant form of VEGF-C that is only able to activate VEGFR-3 strongly promoted metastasis of these cells to the regional lymph nodes and lung [1].
  • CONCLUSION: These data suggest that VEGF-C modulates the proliferative activities of cholangiocytes in experimental cholestasis and that circulating factors (i.e., VEGF) in the blood supply of the intra-hepatic biliary epithelium, play an important role in the balance between cholangiocyte proliferation/loss [2].
  • Lymphatics, which were identified by vascular endothelial growth factor receptor-3 (VEGFR-3) in situ hybridization were absent from C6 gliomas, although a weak expression of the lymphangiogenic growth factor, VEGF-C, could be detected in the C6 cells by Northern blot analysis [3].

High impact information on Vegfc

  • In addition, Vegfc-deficient mouse embryos showed a selective loss of oligodendrocyte precursor cells (OPCs) in the embryonic optic nerve [4].
  • However, tumors derived from cell lines that do not constitutively express VEGF-C or VEGF-D in tissue culture can nevertheless express one or both of these factors [1].
  • We demonstrate that both tumor and stromal cells can contribute to this expression, suggesting that tumor cell-host interactions determine tumor expression of VEGF-C and VEGF-D [1].
  • In the isolated spinal cord preparation, single shock stimulation of a dorsal root at C-fibre strength induced a slow depolarizing response lasting about 30 s (slow ventral root potential; slow VRP) in the ipsilateral ventral root of the same segment [5].
  • VEGF-C was moderately increased during pregnancy and lactation (2- and 3-fold respectively) [6].

Biological context of Vegfc


Anatomical context of Vegfc

  • VEGF, VEGF-C, and VEGFRs -1, -2, and -3 were found to be expressed in post-pubertal (virgin) rodent mammary glands [6].
  • Another NO donor, 3-morpholinosydononimine (SIN-1, 30-300 microM), also depressed the slow VRP but did not depolarize ventral roots [11].
  • The test response was a nociceptive-related slow ventral root potential (slow VRP) recorded from the isolated neonatal rat spinal cord in response to electrical stimulation of a dorsal root [9].
  • In contrast, 10AS cells, which expressed high levels of VEGF-C, induced ingrowth of lymphatics into the tumors, with BrdU-labeling rates of about 9% of lymphatic endothelial cells [3].
  • In immunohistochemical analysis of the rat cornea 3 days after the injury, VEGF-C was mainly detected in inflammatory cells, and VEGFR-3 was demonstrated in several new vessels in the corneal stroma [10].

Associations of Vegfc with chemical compounds

  • The slow VRP depends on both substance P and glutamate NMDA-receptor-mediated neurotransmission; isoflurance and dexmedetomidine depressed responses to both substance P and NMDA [9].
  • Propofol and barbiturate slow VRP depression was antagonized by the GABAA antagonist bicuculline (1 microM) [12].
  • At a lower concentration (0.14 vol%), isoflurane increased the slow VRP in three of five preparations [9].
  • A cyclic GMP-dependent protein kinase inhibitor, KT5823 (0.3 microM), partly inhibited the depressant effects of NO donors and 8-Br-cyclic GMP on the dorsal root-evoked slow VRP [11].
  • RESULTS: Adenosine agonists dose dependently inhibited the slow VRP and the MSR [13].

Other interactions of Vegfc

  • We also synthesized and characterized indolinones that differentially block VEGF-C- and VEGF-D-induced VEGFR-3 kinase activity compared to that of VEGFR-2 [7].
  • Correspondingly, the VEGF-C-specific receptor flt-4 and the VEGF-A receptors flt-1 and flk-1 were up-regulated in a temporal sequence similar to that of their agonist proteins in the cortical ring lesion and the region at risk [14].

Analytical, diagnostic and therapeutic context of Vegfc

  • This study suggests that VEGF-C and its receptor flt-4 may cooperate with VEGF-A and its receptors flt-1 and flk-1 to promote early angiogenesis after stroke, which may in turn contribute to spontaneous reperfusion in this focal thromboembolic stroke model [14].
  • Receptor-based affinity chromatography was used to purify this growth factor, followed by amino acid sequencing and molecular cloning of the murine cDNA, the orthologue of human vascular endothelial growth factor-C and vascular endothelial growth factor related protein [15].


  1. Differential in vivo and in vitro expression of vascular endothelial growth factor (VEGF)-C and VEGF-D in tumors and its relationship to lymphatic metastasis in immunocompetent rats. Krishnan, J., Kirkin, V., Steffen, A., Hegen, M., Weih, D., Tomarev, S., Wilting, J., Sleeman, J.P. Cancer Res. (2003) [Pubmed]
  2. Hepatic microcirculation and cholangiocyte physiopathology. Gaudio, E., Onori, P., Franchitto, A., Pannarale, L., Alpini, G., Alvaro, D. Italian journal of anatomy and embryology = Archivio italiano di anatomia ed embriologia. (2005) [Pubmed]
  3. Interaction of rat tumor cells with blood vessels and lymphatics of the avian chorioallantoic membrane. Papoutsi, M., Sleeman, J.P., Wilting, J. Microsc. Res. Tech. (2001) [Pubmed]
  4. VEGF-C is a trophic factor for neural progenitors in the vertebrate embryonic brain. Le Bras, B., Barallobre, M.J., Homman-Ludiye, J., Ny, A., Wyns, S., Tammela, T., Haiko, P., Karkkainen, M.J., Yuan, L., Muriel, M.P., Chatzopoulou, E., Bréant, C., Zalc, B., Carmeliet, P., Alitalo, K., Eichmann, A., Thomas, J.L. Nat. Neurosci. (2006) [Pubmed]
  5. Involvement of PACAP receptor in primary afferent fibre-evoked responses of ventral roots in the neonatal rat spinal cord. Sakashita, Y., Kurihara, T., Uchida, D., Tatsuno, I., Yamamoto, T. Br. J. Pharmacol. (2001) [Pubmed]
  6. Regulation of VEGF and VEGF receptor expression in the rodent mammary gland during pregnancy, lactation, and involution. Pepper, M.S., Baetens, D., Mandriota, S.J., Di Sanza, C., Oikemus, S., Lane, T.F., Soriano, J.V., Montesano, R., Iruela-Arispe, M.L. Dev. Dyn. (2000) [Pubmed]
  7. Characterization of indolinones which preferentially inhibit VEGF-C- and VEGF-D-induced activation of VEGFR-3 rather than VEGFR-2. Kirkin, V., Mazitschek, R., Krishnan, J., Steffen, A., Waltenberger, J., Pepper, M.S., Giannis, A., Sleeman, J.P. Eur. J. Biochem. (2001) [Pubmed]
  8. Evaluation of stromal metalloproteinases and vascular endothelial growth factors in a spontaneous metastasis model. Donadio, A.C., Durand, S., Remedi, M.M., Frede, S., Ceschin, D.G., Genti-Raimondi, S., Chiabrando, G.A. Exp. Mol. Pathol. (2005) [Pubmed]
  9. Isoflurane and an alpha 2-adrenoceptor agonist suppress nociceptive neurotransmission in neonatal rat spinal cord. Savola, M.K., Woodley, S.J., Maze, M., Kendig, J.J. Anesthesiology (1991) [Pubmed]
  10. Expression of vascular endothelial growth factor C and vascular endothelial growth factor receptor 3 in corneal lymphangiogenesis. Mimura, T., Amano, S., Usui, T., Kaji, Y., Oshika, T., Ishii, Y. Exp. Eye Res. (2001) [Pubmed]
  11. The excitatory and inhibitory modulation of primary afferent fibre-evoked responses of ventral roots in the neonatal rat spinal cord exerted by nitric oxide. Kurihara, T., Yoshioka, K. Br. J. Pharmacol. (1996) [Pubmed]
  12. Propofol and barbiturate depression of spinal nociceptive neurotransmission. Jewett, B.A., Gibbs, L.M., Tarasiuk, A., Kendig, J.J. Anesthesiology (1992) [Pubmed]
  13. Characterization of adenosine receptors mediating spinal sensory transmission related to nociceptive information in the rat. Nakamura, I., Ohta, Y., Kemmotsu, O. Anesthesiology (1997) [Pubmed]
  14. Vascular endothelial growth factor-A and -C protein up-regulation and early angiogenesis in a rat photothrombotic ring stroke model with spontaneous reperfusion. Gu, W., Brännström, T., Jiang, W., Bergh, A., Wester, P. Acta Neuropathol. (2001) [Pubmed]
  15. Characterization of murine Flt4 ligand/VEGF-C. Fitz, L.J., Morris, J.C., Towler, P., Long, A., Burgess, P., Greco, R., Wang, J., Gassaway, R., Nickbarg, E., Kovacic, S., Ciarletta, A., Giannotti, J., Finnerty, H., Zollner, R., Beier, D.R., Leak, L.V., Turner, K.J., Wood, C.R. Oncogene (1997) [Pubmed]
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