Heterogeneity in VEGFR3 levels drives lymphatic vessel hyperplasia through cell-autonomous and non-cell-autonomous mechanisms

VEGF-C is a key regulator of lymphatic development. Here, Zhang et al. show that while complete loss of its receptor VEGFR3 results in vessel hypoplasia, mosaic loss of VEGFR3 leads to hyperplasia through induction of cell proliferation in neighboringnon-targeted cells, uncovering cell- and non-cell...

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Autores principales:	Yan Zhang, Maria H. Ulvmar, Lukas Stanczuk, Ines Martinez-Corral, Maike Frye, Kari Alitalo, Taija Mäkinen
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/68d6077f60da40e9b5ae0351c12303a2
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spelling	oai:doaj.org-article:68d6077f60da40e9b5ae0351c12303a22021-12-02T13:27:23ZHeterogeneity in VEGFR3 levels drives lymphatic vessel hyperplasia through cell-autonomous and non-cell-autonomous mechanisms10.1038/s41467-018-03692-02041-1723https://doaj.org/article/68d6077f60da40e9b5ae0351c12303a22018-04-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-03692-0https://doaj.org/toc/2041-1723VEGF-C is a key regulator of lymphatic development. Here, Zhang et al. show that while complete loss of its receptor VEGFR3 results in vessel hypoplasia, mosaic loss of VEGFR3 leads to hyperplasia through induction of cell proliferation in neighboringnon-targeted cells, uncovering cell- and non-cell-autonomous roles for VEGFR3 during lymphatic vessel growth.Yan ZhangMaria H. UlvmarLukas StanczukInes Martinez-CorralMaike FryeKari AlitaloTaija MäkinenNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-15 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Yan Zhang Maria H. Ulvmar Lukas Stanczuk Ines Martinez-Corral Maike Frye Kari Alitalo Taija Mäkinen Heterogeneity in VEGFR3 levels drives lymphatic vessel hyperplasia through cell-autonomous and non-cell-autonomous mechanisms
description	VEGF-C is a key regulator of lymphatic development. Here, Zhang et al. show that while complete loss of its receptor VEGFR3 results in vessel hypoplasia, mosaic loss of VEGFR3 leads to hyperplasia through induction of cell proliferation in neighboringnon-targeted cells, uncovering cell- and non-cell-autonomous roles for VEGFR3 during lymphatic vessel growth.
format	article
author	Yan Zhang Maria H. Ulvmar Lukas Stanczuk Ines Martinez-Corral Maike Frye Kari Alitalo Taija Mäkinen
author_facet	Yan Zhang Maria H. Ulvmar Lukas Stanczuk Ines Martinez-Corral Maike Frye Kari Alitalo Taija Mäkinen
author_sort	Yan Zhang
title	Heterogeneity in VEGFR3 levels drives lymphatic vessel hyperplasia through cell-autonomous and non-cell-autonomous mechanisms
title_short	Heterogeneity in VEGFR3 levels drives lymphatic vessel hyperplasia through cell-autonomous and non-cell-autonomous mechanisms
title_full	Heterogeneity in VEGFR3 levels drives lymphatic vessel hyperplasia through cell-autonomous and non-cell-autonomous mechanisms
title_fullStr	Heterogeneity in VEGFR3 levels drives lymphatic vessel hyperplasia through cell-autonomous and non-cell-autonomous mechanisms
title_full_unstemmed	Heterogeneity in VEGFR3 levels drives lymphatic vessel hyperplasia through cell-autonomous and non-cell-autonomous mechanisms
title_sort	heterogeneity in vegfr3 levels drives lymphatic vessel hyperplasia through cell-autonomous and non-cell-autonomous mechanisms
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/68d6077f60da40e9b5ae0351c12303a2
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_version_	1718392978833145856

Heterogeneity in VEGFR3 levels drives lymphatic vessel hyperplasia through cell-autonomous and non-cell-autonomous mechanisms

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