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Lookup NU author(s): Professor Helen ArthurORCiD
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
ENDOGLIN (ENG) is a co-receptor for transforming growth factor-beta (TGF-beta) 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.
Author(s): Liu Z, Lebrin F, Maring JA, van den Driesche S, van der Brink S, van Dinther M, Thorikay M, Martin S, Kobayashi K, Hawinkels LJAC, van Meeteren LA, Pardali E, Korving J, Letarte M, Arthur HM, Theuer C, Goumans MJ, Mummery C, ten Dijke P
Publication type: Article
Publication status: Published
Journal: PLoS One
Print publication date: 28/01/2014
Acceptance date: 10/12/2013
Date deposited: 15/04/2014
ISSN (electronic): 1932-6203
Publisher: Public Library of Science
Notes: ARTN e86273
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