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Publication : Role of PFKFB3-driven glycolysis in vessel sprouting.

First Author  De Bock K Year  2013
Journal  Cell Volume  154
Issue  3 Pages  651-63
PubMed ID  23911327 Mgi Jnum  J:200070
Mgi Id  MGI:5506956 Doi  10.1016/j.cell.2013.06.037
Citation  De Bock K, et al. (2013) Role of PFKFB3-Driven Glycolysis in Vessel Sprouting. Cell 154(3):651-63
abstractText  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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