ENDOGLIN is dispensable for vasculogenesis, but required for vascular endothelial growth factor-induced angiogenesis.
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 telan...
| Main Authors: | , , , , , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2014-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3904881?pdf=render |
| _version_ | 1819055482466205696 |
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| author | 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 |
| author_facet | 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 |
| author_sort | Zhen Liu |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-21T13:08:13Z |
| format | Article |
| id | doaj.art-d1ddadd2469b4f18a335f8890b6c45de |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-21T13:08:13Z |
| publishDate | 2014-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-d1ddadd2469b4f18a335f8890b6c45de2022-12-21T19:02:58ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0191e8627310.1371/journal.pone.0086273ENDOGLIN is dispensable for vasculogenesis, but required for vascular endothelial growth factor-induced angiogenesis.Zhen LiuFranck LebrinJanita A MaringSander van den DriescheStieneke van der BrinkMaarten van DintherMidory ThorikaySabrina MartinKazuki KobayashiLukas J A C HawinkelsLaurens A van MeeterenEvangelia PardaliJeroen KorvingMichelle LetarteHelen M ArthurCharles TheuerMarie-José GoumansChristine MummeryPeter ten DijkeENDOGLIN (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.http://europepmc.org/articles/PMC3904881?pdf=render |
| spellingShingle | 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 ENDOGLIN is dispensable for vasculogenesis, but required for vascular endothelial growth factor-induced angiogenesis. PLoS ONE |
| title | ENDOGLIN is dispensable for vasculogenesis, but required for vascular endothelial growth factor-induced angiogenesis. |
| title_full | ENDOGLIN is dispensable for vasculogenesis, but required for vascular endothelial growth factor-induced angiogenesis. |
| title_fullStr | ENDOGLIN is dispensable for vasculogenesis, but required for vascular endothelial growth factor-induced angiogenesis. |
| title_full_unstemmed | ENDOGLIN is dispensable for vasculogenesis, but required for vascular endothelial growth factor-induced angiogenesis. |
| title_short | ENDOGLIN is dispensable for vasculogenesis, but required for vascular endothelial growth factor-induced angiogenesis. |
| title_sort | endoglin is dispensable for vasculogenesis but required for vascular endothelial growth factor induced angiogenesis |
| url | http://europepmc.org/articles/PMC3904881?pdf=render |
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