Motor neurons control blood vessel patterning in the developing spinal cord

Patricia Himmels, Isidora Paredes, Heike Adler, Andromachi Karakatsani, Robert Luck, Hugo H. Marti, Olga Ermakova, Eugen Rempel, Esther T. Stoeckli and Carmen Ruiz de Almodóvar ()
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Patricia Himmels: Biochemistry Center, Heidelberg University
Isidora Paredes: Biochemistry Center, Heidelberg University
Heike Adler: Biochemistry Center, Heidelberg University
Andromachi Karakatsani: Biochemistry Center, Heidelberg University
Robert Luck: Biochemistry Center, Heidelberg University
Hugo H. Marti: Institute of Physiology and Pathophysiology, Heidelberg University
Olga Ermakova: Centre for Organismal Studies, Heidelberg University
Eugen Rempel: Centre for Organismal Studies, Heidelberg University
Esther T. Stoeckli: Institute of Molecular Life Sciences, University of Zurich
Carmen Ruiz de Almodóvar: Biochemistry Center, Heidelberg University

Nature Communications, 2017, vol. 8, issue 1, 1-16

Abstract: Abstract Formation of a precise vascular network within the central nervous system is of critical importance to assure delivery of oxygen and nutrients and for accurate functionality of neuronal networks. Vascularization of the spinal cord is a highly stereotypical process. However, the guidance cues controlling blood vessel patterning in this organ remain largely unknown. Here we describe a new neuro-vascular communication mechanism that controls vessel guidance in the developing spinal cord. We show that motor neuron columns remain avascular during a developmental time window, despite expressing high levels of the pro-angiogenic vascular endothelial growth factor (VEGF). We describe that motor neurons express the VEGF trapping receptor sFlt1 via a Neuropilin-1-dependent mechanism. Using a VEGF gain-of-function approach in mice and a motor neuron-specific sFlt1 loss-of-function approach in chicken, we show that motor neurons control blood vessel patterning by an autocrine mechanism that titrates motor neuron-derived VEGF via their own expression of sFlt1.

Date: 2017
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DOI: 10.1038/ncomms14583

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