Fatty acid carbon is essential for dNTP synthesis in endothelial cells View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-04-01

AUTHORS

Sandra Schoors, Ulrike Bruning, Rindert Missiaen, Karla C. S. Queiroz, Gitte Borgers, Ilaria Elia, Annalisa Zecchin, Anna Rita Cantelmo, Stefan Christen, Jermaine Goveia, Ward Heggermont, Lucica Goddé, Stefan Vinckier, Paul P. Van Veldhoven, Guy Eelen, Luc Schoonjans, Holger Gerhardt, Mieke Dewerchin, Myriam Baes, Katrien De Bock, Bart Ghesquière, Sophia Y. Lunt, Sarah-Maria Fendt, Peter Carmeliet

ABSTRACT

The metabolism of endothelial cells during vessel sprouting remains poorly studied. Here we report that endothelial loss of CPT1A, a rate-limiting enzyme of fatty acid oxidation (FAO), causes vascular sprouting defects due to impaired proliferation, not migration, of human and murine endothelial cells. Reduction of FAO in endothelial cells did not cause energy depletion or disturb redox homeostasis, but impaired de novo nucleotide synthesis for DNA replication. Isotope labelling studies in control endothelial cells showed that fatty acid carbons substantially replenished the Krebs cycle, and were incorporated into aspartate (a nucleotide precursor), uridine monophosphate (a precursor of pyrimidine nucleoside triphosphates) and DNA. CPT1A silencing reduced these processes and depleted endothelial cell stores of aspartate and deoxyribonucleoside triphosphates. Acetate (metabolized to acetyl-CoA, thereby substituting for the depleted FAO-derived acetyl-CoA) or a nucleoside mix rescued the phenotype of CPT1A-silenced endothelial cells. Finally, CPT1 blockade inhibited pathological ocular angiogenesis in mice, suggesting a novel strategy for blocking angiogenesis. More... »

PAGES

192-197

Journal

TITLE

Nature

ISSUE

7546

VOLUME

520

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nature14362

DOI

http://dx.doi.org/10.1038/nature14362

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1030574268

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25830893


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