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

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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Bibliographic Details
Main Authors: Yan Zhang, Maria H. Ulvmar, Lukas Stanczuk, Ines Martinez-Corral, Maike Frye, Kari Alitalo, Taija Mäkinen
Format: Article
Language:English
Published: Nature Publishing Group 2018-04-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-018-03692-0
Description
Summary: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.
ISSN:2041-1723

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