PUBLICATION

The hormonal peptide Elabela guides angioblasts to the midline during vasculogenesis

Authors
Helker, C.S., Schuermann, A., Pollmann, C., Chng, S.C., Kiefer, F., Reversade, B., Herzog, W.
ID
ZDB-PUB-150529-7
Date
2015
Source
eLIFE   4: (Journal)
Registered Authors
Chng, Serene, Helker, Christian, Herzog, Wiebke, REVERSADE, Bruno
Keywords
Vegf, angioblast migration, chemoattractant, developmental biology, dorsal aorta, endothelial cell migration, human biology, medicine, notochord, stem cells, zebrafish
MeSH Terms
  • Animals
  • Cell Movement/physiology*
  • Chemokines/metabolism*
  • Cloning, Molecular
  • DNA Primers/genetics
  • Endothelial Cells/cytology*
  • Endothelial Progenitor Cells/metabolism
  • Endothelial Progenitor Cells/physiology*
  • Humans
  • In Situ Hybridization
  • Models, Biological*
  • Mutagenesis
  • Neovascularization, Physiologic/physiology*
  • Zebrafish
  • Zebrafish Proteins/metabolism*
PubMed
26017639 Full text @ Elife
Abstract
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 (Vegf) 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.
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Human Disease / Model
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