Journal
CELL
Volume 154, Issue 3, Pages 651-663Publisher
CELL PRESS
DOI: 10.1016/j.cell.2013.06.037
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Funding
- FWO
- Emmanuel Vanderschueren fellows of the VLK
- Fondazione Umberto Veronesi
- FWO and Marie Curie Foundation
- Federal Government of Belgium [IUAP7/03]
- Flemish Government (Methusalem funding)
- Concerted Research Activities Belgium [GOA2006/11]
- FWO [G.0652.08, G.0692.09, G.0532.10, G.0817.11, 1.5.202.10.N.00]
- Foundation Leducq Transatlantic Network (ARTEMIS)
- ERC (advanced research grant) [EU-ERC269073]
- Cancer Research UK
- Lister Institute of Preventive Medicine
- ARTEMIS
- ERC [311719]
- HFSP fellowship
- [8,088,385]
- European Research Council (ERC) [311719] Funding Source: European Research Council (ERC)
- Grants-in-Aid for Scientific Research [24657101] Funding Source: KAKEN
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Vessel sprouting by migrating tip and proliferating stalk endothelial cells (ECs) is controlled by genetic signals (such as Notch), but it is unknown whether metabolism also regulates this process. Here, we show that ECs relied on glycolysis rather than on oxidative phosphorylation for ATP production and that loss of the glycolytic activator PFKFB3 in ECs impaired vessel formation. Mechanistically, PFKFB3 not only regulated EC proliferation but also controlled the formation of filopodia/lamellipodia and directional migration, in part by compartmentalizing with F-actin in motile protrusions. Mosaic in vitro and in vivo sprouting assays further revealed that PFKFB3 overexpression overruled the pro-stalk activity of Notch, whereas PFKFB3 deficiency impaired tip cell formation upon Notch blockade, implying that glycolysis regulates vessel branching.
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