ENDOGLIN Is Dispensable for Vasculogenesis, but Required for Vascular Endothelial Growth Factor-Induced Angiogenesis

Z. Liu; F. Lebrin; J. Maring; S. van den Driesche; S. van den Brink; M. van Dinther; M. Thorikay; S. Martin; K. Kobayashi; L. Hawinkels; L.A. van Meeteren; E. Pardali; J. Korving; M. Letarte; H.M. Arthur; C. Theuer; M.J. Goumans; C.L. Hosman - Mummery; P. ten Dijke

ENDOGLIN Is Dispensable for Vasculogenesis, but Required for Vascular Endothelial Growth Factor-Induced Angiogenesis

Translated title of the contribution: ENDOGLIN Is Dispensable for Vasculogenesis, but Required for Vascular Endothelial Growth Factor-Induced Angiogenesis

Z. Liu
, F. Lebrin
, J. Maring
, S. van den Driesche
, S. van den Brink
, M. van Dinther
, M. Thorikay
, S. Martin
, K. Kobayashi
, L. Hawinkels
, L.A. van Meeteren
, E. Pardali
, J. Korving
, M. Letarte
, H.M. Arthur
, C. Theuer
, M.J. Goumans
, C.L. Hosman - Mummery
, P. ten Dijke

Research output: Contribution to journal › Article › Academic › peer-review

Abstract

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

Translated title of the contribution	ENDOGLIN Is Dispensable for Vasculogenesis, but Required for Vascular Endothelial Growth Factor-Induced Angiogenesis
Original language	Undefined/Unknown
Article number	e86273
Pages (from-to)	e86273
Number of pages	1
Journal	PLoS ONE [E]
Volume	9
Issue number	1
Publication status	Published - 2014

Cite this

Liu, Z., Lebrin, F., Maring, J., van den Driesche, S., van den Brink, S., van Dinther, M., Thorikay, M., Martin, S., Kobayashi, K., Hawinkels, L., van Meeteren, L. A., Pardali, E., Korving, J., Letarte, M., Arthur, H. M., Theuer, C., Goumans, M. J., Hosman - Mummery, C. L., & ten Dijke, P. (2014). ENDOGLIN Is Dispensable for Vasculogenesis, but Required for Vascular Endothelial Growth Factor-Induced Angiogenesis. PLoS ONE [E], 9(1), e86273. Article e86273.

@article{8de7488592c14a3b878148253323d253,

title = "ENDOGLIN Is Dispensable for Vasculogenesis, but Required for Vascular Endothelial Growth Factor-Induced Angiogenesis",

abstract = "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 = "Z. Liu and F. Lebrin and J. Maring and \{van den Driesche\}, S. and \{van den Brink\}, S. and \{van Dinther\}, M. and M. Thorikay and S. Martin and K. Kobayashi and L. Hawinkels and \{van Meeteren\}, L.A. and E. Pardali and J. Korving and M. Letarte and H.M. Arthur and C. Theuer and M.J. Goumans and \{Hosman - Mummery\}, C.L. and \{ten Dijke\}, P.",

note = "J AN 28 2014",

year = "2014",

language = "Undefined/Unknown",

volume = "9",

pages = "e86273",

journal = "PLoS ONE [E]",

issn = "1932-6203",

publisher = "Public Library of Science",

number = "1",

}

Liu, Z, Lebrin, F, Maring, J, van den Driesche, S, van den Brink, S, van Dinther, M, Thorikay, M, Martin, S, Kobayashi, K, Hawinkels, L, van Meeteren, LA, Pardali, E, Korving, J, Letarte, M, Arthur, HM, Theuer, C, Goumans, MJ, Hosman - Mummery, CL & ten Dijke, P 2014, 'ENDOGLIN Is Dispensable for Vasculogenesis, but Required for Vascular Endothelial Growth Factor-Induced Angiogenesis', PLoS ONE [E], vol. 9, no. 1, e86273, pp. e86273.

TY - JOUR

T1 - ENDOGLIN Is Dispensable for Vasculogenesis, but Required for Vascular Endothelial Growth Factor-Induced Angiogenesis

AU - Liu, Z.

AU - Lebrin, F.

AU - Maring, J.

AU - van den Driesche, S.

AU - van den Brink, S.

AU - van Dinther, M.

AU - Thorikay, M.

AU - Martin, S.

AU - Kobayashi, K.

AU - Hawinkels, L.

AU - van Meeteren, L.A.

AU - Pardali, E.

AU - Korving, J.

AU - Letarte, M.

AU - Arthur, H.M.

AU - Theuer, C.

AU - Goumans, M.J.

AU - Hosman - Mummery, C.L.

AU - ten Dijke, P.

N1 - J AN 28 2014

PY - 2014

Y1 - 2014

N2 - 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

AB - 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

M3 - Article

SN - 1932-6203

VL - 9

SP - e86273

JO - PLoS ONE [E]

JF - PLoS ONE [E]

IS - 1

M1 - e86273

ER -

ENDOGLIN Is Dispensable for Vasculogenesis, but Required for Vascular Endothelial Growth Factor-Induced Angiogenesis

Abstract

Fingerprint

Cite this