Neuronal sFlt1 and Vegfaa determine venous sprouting and spinal cord vascularization

Raphael Wild, Alina Klems, Masanari Takamiya, Yuya Hayashi, Uwe Strähle, Koji Ando, Naoki Mochizuki, Andreas van Impel, Stefan Schulte-Merker, Janna Krueger, Laetitia Preau and Ferdinand le Noble ()
Additional contact information
Raphael Wild: Institute of Zoology (ZOO) Karlsruhe Institute of Technology (KIT)
Alina Klems: Institute of Zoology (ZOO) Karlsruhe Institute of Technology (KIT)
Masanari Takamiya: Institute for Toxicology and Genetics (ITG), Karlsruhe Institute of Technology (KIT)
Yuya Hayashi: Institute for Toxicology and Genetics (ITG), Karlsruhe Institute of Technology (KIT)
Uwe Strähle: Institute for Toxicology and Genetics (ITG), Karlsruhe Institute of Technology (KIT)
Koji Ando: National Cerebral and Cardiovascular Research Institute
Naoki Mochizuki: National Cerebral and Cardiovascular Research Institute
Andreas van Impel: Institute for Cardiovascular Organogenesis and Regeneration, Faculty of Medicine, University of Münster
Stefan Schulte-Merker: Institute for Cardiovascular Organogenesis and Regeneration, Faculty of Medicine, University of Münster
Janna Krueger: Biological Sciences Platform, Sunnybrook Research Institute
Laetitia Preau: Institute of Zoology (ZOO) Karlsruhe Institute of Technology (KIT)
Ferdinand le Noble: Institute of Zoology (ZOO) Karlsruhe Institute of Technology (KIT)

Nature Communications, 2017, vol. 8, issue 1, 1-17

Abstract: Abstract Formation of organ-specific vasculatures requires cross-talk between developing tissue and specialized endothelial cells. Here we show how developing zebrafish spinal cord neurons coordinate vessel growth through balancing of neuron-derived Vegfaa, with neuronal sFlt1 restricting Vegfaa-Kdrl mediated angiogenesis at the neurovascular interface. Neuron-specific loss of flt1 or increased neuronal vegfaa expression promotes angiogenesis and peri-neural tube vascular network formation. Combining loss of neuronal flt1 with gain of vegfaa promotes sprout invasion into the neural tube. On loss of neuronal flt1, ectopic sprouts emanate from veins involving special angiogenic cell behaviours including nuclear positioning and a molecular signature distinct from primary arterial or secondary venous sprouting. Manipulation of arteriovenous identity or Notch signalling established that ectopic sprouting in flt1 mutants requires venous endothelium. Conceptually, our data suggest that spinal cord vascularization proceeds from veins involving two-tiered regulation of neuronal sFlt1 and Vegfaa via a novel sprouting mode.

Date: 2017
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DOI: 10.1038/ncomms13991

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