The hormonal peptide Elabela guides angioblasts to the midline during vasculogenesis

Autor: Bruno Reversade, Annika Schuermann, Cathrin Pollmann, Friedemann Kiefer, Serene C Chng, Wiebke Herzog, Christian S. M. Helker
Přispěvatelé: Center for Reproductive Medicine
Jazyk: angličtina
Rok vydání: 2015
Předmět:
Angioblast
chemistry.chemical_compound
Dorsal aorta
Cell Movement
Biology (General)
Cloning
Molecular

In Situ Hybridization
Zebrafish
Endothelial Progenitor Cells
General Neuroscience
angioblast migration
chemoattractant
notochord
General Medicine
Apelin
Cell biology
Vascular endothelial growth factor
medicine.anatomical_structure
Circulatory system
cardiovascular system
Medicine
Chemokines
endothelial cell migration
dorsal aorta
Blood vessel
medicine.medical_specialty
QH301-705.5
Science
Short Report
Neovascularization
Physiologic

Biology
Models
Biological

Vegf
General Biochemistry
Genetics and Molecular Biology

Vasculogenesis
Internal medicine
medicine
Animals
Humans
Human Biology and Medicine
DNA Primers
Apelin receptor
General Immunology and Microbiology
Endothelial Cells
Zebrafish Proteins
Developmental Biology and Stem Cells
Endocrinology
chemistry
Mutagenesis
Zdroj: eLife
eLife, 4. eLife Sciences Publications
eLife, Vol 4 (2015)
ISSN: 2050-084X
DOI: 10.7554/elife.06726
Popis: 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. DOI: http://dx.doi.org/10.7554/eLife.06726.001
eLife digest The circulatory system enables blood to move around the body and deliver substances including nutrients and oxygen to the cells that need them. In the embryos of animals with a backbone, blood flows from the heart through the aorta into branching smaller vessels to the cells. The blood then gets collected by progressively bigger vessels and flows back to the heart via the cardinal vein. The cells that make up these blood vessels develop from cells called angioblasts—but first, during development these angioblasts must move to the place where the vessels will form. A protein called Vascular endothelial growth factor (VEGF) had been suggested to help guide and align the angioblasts as the embryo develops. Now, Helker, Schuermann et al. have examined developing zebrafish embryos using new technologies. This revealed that VEGF is in fact not essential for the dorsal aorta and cardinal vein to develop. Instead, the angioblasts only move to the correct part of the embryo if they can produce the Apelin receptor protein, which forms part of a signaling pathway. There are two hormones—called Apelin and Elabela—that can bind to and activate the Apelin receptor. Helker, Schuermann et al. show that Elabela alone is needed to guide the angioblasts to the right part of the embryo during blood vessel development. However, in embryos where there is not enough Elabela, the Apelin hormone can compensate for this deficiency and the first blood vessels will later develop correctly. Future research will address whether this signaling pathway not only guides angioblasts to establish a circulatory system, but also guides blood vessel growth. As blood vessel growth is very relevant to human disease, identifying the mechanisms that regulate it will have an impact on biomedical research. DOI: http://dx.doi.org/10.7554/eLife.06726.002
Databáze: OpenAIRE