The hormonal peptide Elabela guides angioblasts to the midline during vasculogenesis
Christian SM Helker,
Annika Schuermann,
Cathrin Pollmann,
Serene C Chng,
Friedemann Kiefer,
Bruno Reversade,
Wiebke Herzog
Affiliations
Christian SM Helker
University of Muenster, Muenster, Germany
Annika Schuermann
University of Muenster, Muenster, Germany
Cathrin Pollmann
Max Planck Institute for Molecular Biomedicine, Muenster, Germany
Serene C Chng
Institute of Medical Biology, Human Genetics and Embryology Laboratory, A*STAR, Singapore, Singapore
Friedemann Kiefer
Max Planck Institute for Molecular Biomedicine, Muenster, Germany; Cells-in-Motion Cluster of Excellence, University of Muenster, Muenster, Germany
Bruno Reversade
Institute of Medical Biology, Human Genetics and Embryology Laboratory, A*STAR, Singapore, Singapore
Wiebke Herzog
University of Muenster, Muenster, Germany; Max Planck Institute for Molecular Biomedicine, Muenster, Germany; Cells-in-Motion Cluster of Excellence, University of Muenster, Muenster, Germany
A key step in the de novo formation of the embryonic vasculature is the migration of endothelial precursors, the angioblasts, to the position of the future vessels. To form the first axial vessels, angioblasts migrate towards the midline and coalesce underneath the notochord. Vascular endothelial growth factor has been proposed to serve as a chemoattractant for the angioblasts and to regulate this medial migration. Here we challenge this model and instead demonstrate that angioblasts rely on their intrinsic expression of Apelin receptors (Aplr, APJ) for their migration to the midline. We further show that during this angioblast migration Apelin receptor signaling is mainly triggered by the recently discovered ligand Elabela (Ela). As neither of the ligands Ela or Apelin (Apln) nor their receptors have previously been implicated in regulating angioblast migration, we hereby provide a novel mechanism for regulating vasculogenesis, with direct relevance to physiological and pathological angiogenesis.
