Glycolytic regulation of cell rearrangement in angiogenesis

Bert Cruys, Brian W. Wong, Anna Kuchnio, Dries Verdegem, Anna Rita Cantelmo, Lena-Christin Conradi, Saar Vandekeere, Ann Bouché, Ivo Cornelissen, Stefan Vinckier, Roeland M. H. Merks, Elisabetta Dejana, Holger Gerhardt, Mieke Dewerchin, Katie Bentley () and Peter Carmeliet ()
Additional contact information
Bert Cruys: Laboratory of Angiogenesis and Vascular Metabolism
Brian W. Wong: Laboratory of Angiogenesis and Vascular Metabolism
Anna Kuchnio: Laboratory of Angiogenesis and Vascular Metabolism
Dries Verdegem: Laboratory of Angiogenesis and Vascular Metabolism
Anna Rita Cantelmo: Laboratory of Angiogenesis and Vascular Metabolism
Lena-Christin Conradi: Laboratory of Angiogenesis and Vascular Metabolism
Saar Vandekeere: Laboratory of Angiogenesis and Vascular Metabolism
Ann Bouché: Laboratory of Angiogenesis and Vascular Metabolism
Ivo Cornelissen: Laboratory of Angiogenesis and Vascular Metabolism
Stefan Vinckier: Laboratory of Angiogenesis and Vascular Metabolism
Roeland M. H. Merks: Life Sciences Group, Centrum Wiskunde and Informatica
Elisabetta Dejana: Genetics and Pathology, Rudbeck Laboratory, Uppsala University
Holger Gerhardt: Vascular Patterning Laboratory
Mieke Dewerchin: Laboratory of Angiogenesis and Vascular Metabolism
Katie Bentley: Genetics and Pathology, Rudbeck Laboratory, Uppsala University
Peter Carmeliet: Laboratory of Angiogenesis and Vascular Metabolism

Nature Communications, 2016, vol. 7, issue 1, 1-15

Abstract: Abstract During vessel sprouting, endothelial cells (ECs) dynamically rearrange positions in the sprout to compete for the tip position. We recently identified a key role for the glycolytic activator PFKFB3 in vessel sprouting by regulating cytoskeleton remodelling, migration and tip cell competitiveness. It is, however, unknown how glycolysis regulates EC rearrangement during vessel sprouting. Here we report that computational simulations, validated by experimentation, predict that glycolytic production of ATP drives EC rearrangement by promoting filopodia formation and reducing intercellular adhesion. Notably, the simulations correctly predicted that blocking PFKFB3 normalizes the disturbed EC rearrangement in high VEGF conditions, as occurs during pathological angiogenesis. This interdisciplinary study integrates EC metabolism in vessel sprouting, yielding mechanistic insight in the control of vessel sprouting by glycolysis, and suggesting anti-glycolytic therapy for vessel normalization in cancer and non-malignant diseases.

Date: 2016
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DOI: 10.1038/ncomms12240

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