Endothelial cells by inactivation of VHL gene direct angiogenesis, not vasculogenesis via Twist1 accumulation associated with hemangioblastoma neovascularization

Abstract Inactivation of the VHL tumour suppressor gene is a highly frequent genetic event in the carcinogenesis of central nervous system-(CNS) hemangioblastomas (HBs). The patterning of the similar embryonic vasculogenesis is an increasing concern in HB-neovascularization, and the classic vascular...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Ying Wang, Dan-Qi Chen, Ming-Yu Chen, Kai-Yuan Ji, De-Xuan Ma, Liang-Fu Zhou
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/6de1c79e46e64f20b1b312162d729d6d
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:6de1c79e46e64f20b1b312162d729d6d
record_format	dspace
spelling	oai:doaj.org-article:6de1c79e46e64f20b1b312162d729d6d2021-12-02T11:52:41ZEndothelial cells by inactivation of VHL gene direct angiogenesis, not vasculogenesis via Twist1 accumulation associated with hemangioblastoma neovascularization10.1038/s41598-017-05833-92045-2322https://doaj.org/article/6de1c79e46e64f20b1b312162d729d6d2017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-05833-9https://doaj.org/toc/2045-2322Abstract Inactivation of the VHL tumour suppressor gene is a highly frequent genetic event in the carcinogenesis of central nervous system-(CNS) hemangioblastomas (HBs). The patterning of the similar embryonic vasculogenesis is an increasing concern in HB-neovascularization, and the classic vascular endothelial growth factor (VEGF)-mediated angiogenesis driven by VHL loss-of-function from human endothelium have been questioned. With this regard, we identify a distinct, VHL silencing-driven mechanism in which human vascular endothelial cells by means of increasing cell proliferation and decreasing cell apoptosis, is concomitant with facilitating accumulation of Twist1 protein in vascular endothelial cells in vitro. Importantly, this molecular mechanism is also pinpointed in CNS-HBs, and associated with the process of HB-neovascularization. In contrast with recent studies of HB-neovascularization, these modified cells did not endow with the typical features of vasculogenesis, indicating that this is a common angiogenesis implementing the formation of the vascular network. Taken together, these findings suggest that vasculogenesis and angiogenesis may constitute complementary mechanisms for HB-neovascularization, and could provide a rational recognition of single anti-angiogenic intervention including targeting to the Twist1 signalling for HBs.Ying WangDan-Qi ChenMing-Yu ChenKai-Yuan JiDe-Xuan MaLiang-Fu ZhouNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ying Wang Dan-Qi Chen Ming-Yu Chen Kai-Yuan Ji De-Xuan Ma Liang-Fu Zhou Endothelial cells by inactivation of VHL gene direct angiogenesis, not vasculogenesis via Twist1 accumulation associated with hemangioblastoma neovascularization
description	Abstract Inactivation of the VHL tumour suppressor gene is a highly frequent genetic event in the carcinogenesis of central nervous system-(CNS) hemangioblastomas (HBs). The patterning of the similar embryonic vasculogenesis is an increasing concern in HB-neovascularization, and the classic vascular endothelial growth factor (VEGF)-mediated angiogenesis driven by VHL loss-of-function from human endothelium have been questioned. With this regard, we identify a distinct, VHL silencing-driven mechanism in which human vascular endothelial cells by means of increasing cell proliferation and decreasing cell apoptosis, is concomitant with facilitating accumulation of Twist1 protein in vascular endothelial cells in vitro. Importantly, this molecular mechanism is also pinpointed in CNS-HBs, and associated with the process of HB-neovascularization. In contrast with recent studies of HB-neovascularization, these modified cells did not endow with the typical features of vasculogenesis, indicating that this is a common angiogenesis implementing the formation of the vascular network. Taken together, these findings suggest that vasculogenesis and angiogenesis may constitute complementary mechanisms for HB-neovascularization, and could provide a rational recognition of single anti-angiogenic intervention including targeting to the Twist1 signalling for HBs.
format	article
author	Ying Wang Dan-Qi Chen Ming-Yu Chen Kai-Yuan Ji De-Xuan Ma Liang-Fu Zhou
author_facet	Ying Wang Dan-Qi Chen Ming-Yu Chen Kai-Yuan Ji De-Xuan Ma Liang-Fu Zhou
author_sort	Ying Wang
title	Endothelial cells by inactivation of VHL gene direct angiogenesis, not vasculogenesis via Twist1 accumulation associated with hemangioblastoma neovascularization
title_short	Endothelial cells by inactivation of VHL gene direct angiogenesis, not vasculogenesis via Twist1 accumulation associated with hemangioblastoma neovascularization
title_full	Endothelial cells by inactivation of VHL gene direct angiogenesis, not vasculogenesis via Twist1 accumulation associated with hemangioblastoma neovascularization
title_fullStr	Endothelial cells by inactivation of VHL gene direct angiogenesis, not vasculogenesis via Twist1 accumulation associated with hemangioblastoma neovascularization
title_full_unstemmed	Endothelial cells by inactivation of VHL gene direct angiogenesis, not vasculogenesis via Twist1 accumulation associated with hemangioblastoma neovascularization
title_sort	endothelial cells by inactivation of vhl gene direct angiogenesis, not vasculogenesis via twist1 accumulation associated with hemangioblastoma neovascularization
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/6de1c79e46e64f20b1b312162d729d6d
work_keys_str_mv	AT yingwang endothelialcellsbyinactivationofvhlgenedirectangiogenesisnotvasculogenesisviatwist1accumulationassociatedwithhemangioblastomaneovascularization AT danqichen endothelialcellsbyinactivationofvhlgenedirectangiogenesisnotvasculogenesisviatwist1accumulationassociatedwithhemangioblastomaneovascularization AT mingyuchen endothelialcellsbyinactivationofvhlgenedirectangiogenesisnotvasculogenesisviatwist1accumulationassociatedwithhemangioblastomaneovascularization AT kaiyuanji endothelialcellsbyinactivationofvhlgenedirectangiogenesisnotvasculogenesisviatwist1accumulationassociatedwithhemangioblastomaneovascularization AT dexuanma endothelialcellsbyinactivationofvhlgenedirectangiogenesisnotvasculogenesisviatwist1accumulationassociatedwithhemangioblastomaneovascularization AT liangfuzhou endothelialcellsbyinactivationofvhlgenedirectangiogenesisnotvasculogenesisviatwist1accumulationassociatedwithhemangioblastomaneovascularization
_version_	1718394990560804864

Endothelial cells by inactivation of VHL gene direct angiogenesis, not vasculogenesis via Twist1 accumulation associated with hemangioblastoma neovascularization

Ejemplares similares