Endothelial signalling by the Notch ligand Delta-like 4 restricts angiogenesis

被引:323
|
作者
Leslie, Jonathan D.
Ariza-McNaughton, Linda
Bermange, Adam L.
McAdow, Ryan
Johnson, Stephen L.
Lewis, Julian
机构
[1] Canc Res UK London Res Inst, Vertebrate Dev Lab, London WC2A 3PX, England
[2] Washington Univ, Sch Med, Dept Genet, St Louis, MO 63110 USA
来源
DEVELOPMENT | 2007年 / 134卷 / 05期
关键词
Notch; Delta-like; 4; angiogenesis; endothelial; motility; zebrafish; INHIBITS TUMOR-GROWTH; VASCULAR DEVELOPMENT; ACTIVATED NOTCH4; UP-REGULATION; CELL FUNCTION; ZEBRAFISH; ARTERIAL; EXPRESSION; DLL4; DIFFERENTIATION;
D O I
10.1242/dev.003244
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Notch signalling by the ligand Delta-like 4 (DII4) is essential for normal vascular remodelling, yet the precise way in which the pathway influences the behaviour of endothelial cells remains a mystery. Using the embryonic zebrafish, we show that, when DII4-Notch signalling is defective, endothelial cells continue to migrate and proliferate when they should normally stop these processes. Artificial overactivation of the Notch pathway has opposite consequences. When vascular endothelial growth factor (Vegf) signalling and DII4-Notch signalling are both blocked, the endothelial cells remain quiescent. Thus, DII4-Notch signalling acts as an angiogenic 'off' switch by making endothelial cells unresponsive to Vegf.
引用
收藏
页码:839 / 844
页数:6
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