Human VEGF-C and VEGF-D

SABio is an official partner in distribution of Human Recombinant VEGF-C and VEGF-D products from Vegenics Pty Ltd..

VEGENICS is an emerging leader in the field of angiogenesis focusing on a class of drug targets called Vascular Endothelial Growth Factors (VEGFs). Vegenics owns the world’s largest and most comprehensive intellectual property estate covering the key angiogenesis targets VEGF-C, VEGF-D and VEGFR-3. The products are intended for research use only.

For enquiries and quotations, please  contact us at [email protected] .

We deliver in Singapore within 24 hours free of charge.

SABio is an official distributor of
25 ug recombinant Human VEGF-C
Catalogue Number: VC_025

Research use only.
25 ug recombinant Human VEGF-D
Catalogue Number: VD_025

Research use only.
Anti Human VEGF-D Antibody
Catalogue Number: mAb VD-1

Research use only.
5 ug recombinant Human VEGF-D
Catalogue Number: VD_005

Research use only.
About VEGF-C

VEGF-C is a member of the VEGF family of secreted glycoprotein that are critical mediators of angiogenesis and lymphangiogenesis1,2. The VEGFs bind to VEGFR-1 (Flt-1), VEGFR-2 (KDR/Flk-1) and VEGFR-3 (Flt-4), a family of structurally related receptor tyrosine kinases that are predominantly expressed on the endothelial cells of blood and/or lymphatic vessels1. The VEGFs have distinct receptor binding specificities which contribute to their diversity of function. VEGF-C was first described in 1996 by Vegenics collaborators in the Laboratory of Prof. Kari Alitalo3. VEGF-C is synthesised as an immature protein consisting of the receptor binding domain (VEGF homology domain, VHD) flanked by amino and carboxyl-terminal propetides3. During secretion, the immature protein undergoes proteolytic processing to remove the propeptides, yielding the mature form of the protein, a VHD homodimer4. As a consequence of processing the affinity of the mature form of VEGF-C for its receptors is substantially increased4. VEGF-C induces angiogenesis via the activation of both VEGFR-2 and VEGFR-3, and lymphangiogenesis via activation of VEGFR-3. VEGF-C stimulates proliferation of endothelial cells in vitro4 and induces angiogenesis in several in vivo models5-7.  VEGF-C is essential during embryonic formation of the lymphatic system8, whereas in the adult its expression is down regulated in normal tissues and up regulated in pathological states that require the formation of vascular and/or lymphatatic network, including wound healing and tumor growth9,10. Indeed high expression levels of VEGF-C in human colorectal11,12, lung13, breast14, gastric15 and pancreatic16 cancers indicates that increased expression of VEGF-C correlates with greater tumour aggression and a poorer prognosis.

References

  1. Tammela, T., et al., The biology of vascular endothelial growth factors. Cardiovasc Res, 2005. 65(3): p. 550-63.
  2. Adams, R.H. and K. Alitalo, Molecular regulation of angiogenesis and lymphangiogenesis. Nat Rev Mol Cell Biol, 2007. 8(6): p. 464-78.
  3. Joukov, V., et al., A novel vascular endothelial growth factor, VEGF-C, is a ligand for the Flt4 (VEGFR-3) and KDR (VEGFR-2) receptor tyrosine kinases. EMBO J, 1996. 15(2): p. 290-98.
  4. Joukov, V., et al., Proteolytic processing regulates receptor specificity and activity of VEGF-C. EMBO J, 1997. 16(13): p. 3898-911.
  5. Cao, Y., et al., Vascular endothelial growth factor C induces angiogenesis in vivo. Proc Natl Acad Sci U S A, 1998. 95(24): p. 14389-94.
  6. Witzenbichler, B., et al., Vascular endothelial growth factor-C (VEGF-C/VEGF-2) promotes angiogenesis in the setting of tissue ischemia. Am J Pathol, 1998. 153(2): p. 381-94.
  7. Chung, E.S., et al., Contribution of macrophages to angiogenesis induced by vascular endothelial growth factor receptor-3-specific ligands. Am J Pathol, 2009. 175(5): p. 1984-92.
  8. Karkkainen, M.J., et al., Vascular endothelial growth factor C is required for sprouting of the first lymphatic vessels from embryonic veins. Nat Immunol, 2004. 5(1): p. 74-80.
  9. Witmer, A.N., et al., VEGFR-3 in adult angiogenesis. J Pathol, 2001. 195(4): p. 490-7.
  10. Tammela, T., et al., Blocking VEGFR-3 suppresses angiogenic sprouting and vascular network formation. Nature, 2008. 454(7204): p. 656-60.
  11. Akagi, K., et al., Vascular endothelial growth factor-C (VEGF-C) expression in human colorectal cancer tissues. Br J Cancer, 2000. 83(7): p. 887-91.
  12. Onogawa, S., et al., Expression of VEGF-C and VEGF-D at the invasive edge correlates with lymph node metastasis and prognosis of patients with colorectal carcinoma. Cancer Sci, 2004. 95(1): p. 32-9.
  13. Takizawa, H., et al., The balance of VEGF-C and VEGFR-3 mRNA is a predictor of lymph node metastasis in non-small cell lung cancer. Br J Cancer, 2006. 95(1): p. 75-9.
  14. Mohammed, R.A., et al., Prognostic significance of vascular endothelial cell growth factors -A, -C and -D in breast cancer and their relationship with angio- and lymphangiogenesis. Br J Cancer, 2007. 96(7): p. 1092-100.
  15. Morita, H., et al., Histopathological predictor for regional lymph node metastasis in gastric cancer. Virchows Arch, 2009. 454(2): p. 143-51.
  16. Kurahara, H., et al., Impact of vascular endothelial growth factor-C and -D expression in human pancreatic cancer: its relationship to lymph node metastasis. Clin Cancer Res, 2004. 10(24): p. 8413-20.
About VEGF-D

VEGF-D is a member of the VEGF family of secreted glycoproteins that are critical mediators of angiogenesis and lymphangiogenesis2,3. The VEGFs bind to VEGFR-1 (Flt-1), VEGFR-2 (KDR/Flk-1) and VEGFR-3 (Flt-4), a family of structurally related receptor tyrosine kinases that are predominantly expressed on the endothelial cells of blood and/or lymphatic vessels2. The VEGFs have distinct receptor binding specificities which contribute to their diversity of function. VEGF-D was first described in the mouse as a c-fos-induced growth factor (FIGF)4 and subsequently identified in the human1. VEGF-D is synthesised as an immature protein consisting of the receptor binding domain (VEGF homology domain, VHD) flanked by amino and carboxyl-terminal propeptides1. Proteolytic processing by serine proteinases including plasmin5 and proprotein convertases6 remove both propeptides to yield the mature form of the protein, a VHD homodimer. As a consequence of processing the affinity of the mature form of VEGF-D for its receptors is substantially increased7. VEGF-D induces angiogenesis via the activation of both VEGFR-2 and VEGFR-3, and lymphangiogenesis via activation of VEGFR-3. VEGF­D is expressed in adult lung, heart, muscle and small intestine, and is most abundantly expressed in foetal lungs and skin7,8, where it is thought play a modifying role in lymphangiogenesis during embryonic development. In the cancer setting VEGF-D promotes solid tumor growth and lymph node metastasis9, and is a poor prognostic marker for colorectal10, ovarian11, prostate12, gastric13 and lung14 cancers. In addition VEGF-D has been shown to have a role in the lung disease Lymphangioleiomyomatosis (LAM) and is a marker for evaluating disease severity15,16.

 References

  1. Achen M, et al. (1998) Vascular endothelial growth factor D (VEGF-D) is a ligand for the tyrosine kinases VEGF receptor 2 (Flk1) and VEGF receptor 3 (Flt4). Proc. Natl. Acad. Sci.95 (2):548–553.
  2. Veikkola T, et al (2001) Signalling via vascular endothelial growth factor receptor-3 is sufficient for lymphangiogenesis in transgenic mice. EMBO J. (20):1223-1231.
  3. Rissanen, T, et al. (2003) VEGF-D is the strongest angiogenic and lymphangiogenic effector among VEGF delivered into skeletal muscle via adenoviruses. Circ Res 92: 1098-1106.
  4. Orlandini M, et al. (1996). Identification of a c-fos-induced gene that is related to the platelet-derived growth factor/vascular endothelial growth factor family. Proc. Natl. Acad. Sci. USA 93(21):11675-11680.
  5. McColl, B. et al. (2003) Plasmin activates the lymphangiogenic growth factors VEGF-C  and VEGF-D. J. Exp. Med. 198:863-868.
  6. McColl, B. et al. (2007) Proprotein convertases promote processing of VEGF-D, a critical step for binding the angiogenic receptor VEGFR-2. FASEB J. 21:1088-1098.
  7. Stacker SA, et al. (1999) Biosynthesis of Vascular Endothelial Growth Factor-D Involves Proteolytic Processing Which Generates Non-covalent Homodimers. J Biol Chem. 274(45): 32127–32136.
  8. Roy H, et al.  (2006) Biology of vascular endothelial growth factors. FEBS Lett 580:2879–87.
  9. Stacker SA, et al. (2001) VEGF-D promotes the metastatic spread of tumor cells via the lymphatics. Nature Medicine 7 (2):186-191.
  10. White, J. et al. (2002) Vascular endothelial growth factor-D expression is an independent prognostic marker for survival in colorectal carcinoma. Cancer Res. 62:1669-1675.
  11. Yokoyama, Y. et al. (2003) Vascular endothelial growth factor-D expression is an independent prognostic marker for survival in epithelial ovarian carcinoma. Br. J. Cancer 88: 237-244.
  12. Stearns, M. et al. (2004) Expression of a flt-4 (VEGFR3) splicing variant in primary human prostate tumors. VEGF D and flt-4t(Delta773-1081) overexpression is diagnostic for sentinel lymph node metastasis. Lab. Invest. 84: 785-795.
  13. Schimanski, C. et al. (2011) VEGF-D correlates with metastatic disease in gastric cancer patients undergoing surgery. World J. Surgery 35(5): 1010-1016.
  14. Bo. C. et al. (2009) Expression of vascular endothelial growth factors C and D correlates with lymphangiogenesis and lymph node metastasis in lung adenocarcinoma. Thoracic Cardio. Surgeon. 57(5): 291-294.
  15. Seyama, K. et al. (2006) Vascular endothelial growth factor-D is increased in serum of patients with lymphangioleiomyomatosis. Lymphat. Res. Biol. 4:143-152.
  16. Glasgow, C. et al. (2009) Serum vascular endothelial growth factor-D levels in patients with lymphangioleiomyomatosis reflect lymphatic involvement. Chest 135: 1293-1300.

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