ENDOGLIN is dispensable for vasculogenesis, but required for vascular endothelial growth factor-induced angiogenesis

Zhen Liu, Franck Lebrin, Janita A Maring, Sander van den Driesche, Stieneke van der Brink, Maarten van Dinther, Midory Thorikay, Sabrina Martin, Kazuki Kobayashi, Lukas J A C Hawinkels, Laurens A van Meeteren, Evangelia Pardali, Jeroen Korving, Michelle Letarte, Helen M Arthur, Charles Theuer, Marie-José Goumans, Christine Mummery, Peter ten Dijke

Research output: Contribution to journalArticlepeer-review

Abstract

ENDOGLIN (ENG) is a co-receptor for transforming growth factor-β (TGF-β) family members that is highly expressed in endothelial cells and has a critical function in the development of the vascular system. Mutations in Eng are associated with the vascular disease known as hereditary hemorrhagic telangiectasia type l. Using mouse embryonic stem cells we observed that angiogenic factors, including vascular endothelial growth factor (VEGF), induce vasculogenesis in embryoid bodies even when Eng deficient cells or cells depleted of Eng using shRNA are used. However, ENG is required for the stem cell-derived endothelial cells to organize effectively into tubular structures. Consistent with this finding, fetal metatarsals isolated from E17.5 Eng heterozygous mouse embryos showed reduced VEGF-induced vascular network formation. Moreover, shRNA-mediated depletion and pharmacological inhibition of ENG in human umbilical vein cells mitigated VEGF-induced angiogenesis. In summary, we demonstrate that ENG is required for efficient VEGF-induced angiogenesis.

Original languageEnglish
Pages (from-to)e86273
JournalPLoS ONE
Volume9
Issue number1
DOIs
Publication statusPublished - 28 Jan 2014

Keywords

  • Animals
  • Cell Differentiation
  • Flow Cytometry
  • Fluorescent Antibody Technique
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Intracellular Signaling Peptides and Proteins
  • Mice
  • Neovascularization, Physiologic
  • Vascular Endothelial Growth Factor A

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