Coronary vasculature patterning requires a novel endothelial ErbB2 holoreceptor
Haig Aghajanian,
Young Kuk Cho,
Lauren J. Manderfield,
Madison R. Herling,
Mudit Gupta,
Vivienne C. Ho,
Li Li,
Karl Degenhardt,
Alla Aharonov,
Eldad Tzahor and
Jonathan A. Epstein ()
Additional contact information
Haig Aghajanian: Penn Cardiovascular Institute, Institute for Regenerative Medicine, Perelman School of Medicine at the University of Pennsylvania
Young Kuk Cho: Penn Cardiovascular Institute, Institute for Regenerative Medicine, Perelman School of Medicine at the University of Pennsylvania
Lauren J. Manderfield: Penn Cardiovascular Institute, Institute for Regenerative Medicine, Perelman School of Medicine at the University of Pennsylvania
Madison R. Herling: Penn Cardiovascular Institute, Institute for Regenerative Medicine, Perelman School of Medicine at the University of Pennsylvania
Mudit Gupta: Penn Cardiovascular Institute, Institute for Regenerative Medicine, Perelman School of Medicine at the University of Pennsylvania
Vivienne C. Ho: Penn Cardiovascular Institute, Institute for Regenerative Medicine, Perelman School of Medicine at the University of Pennsylvania
Li Li: Penn Cardiovascular Institute, Institute for Regenerative Medicine, Perelman School of Medicine at the University of Pennsylvania
Karl Degenhardt: Children’s Hospital of Philadelphia, University of Pennsylvania
Alla Aharonov: Weizmann Institute of Science
Eldad Tzahor: Weizmann Institute of Science
Jonathan A. Epstein: Penn Cardiovascular Institute, Institute for Regenerative Medicine, Perelman School of Medicine at the University of Pennsylvania
Nature Communications, 2016, vol. 7, issue 1, 1-9
Abstract:
Abstract Organogenesis and regeneration require coordination of cellular proliferation, regulated in part by secreted growth factors and cognate receptors, with tissue nutrient supply provided by expansion and patterning of blood vessels. Here we reveal unexpected combinatorial integration of a growth factor co-receptor with a heterodimeric partner and ligand known to regulate angiogenesis and vascular patterning. We show that ErbB2, which can mediate epidermal growth factor (EGF) and neuregulin signalling in multiple tissues, is unexpectedly expressed by endothelial cells where it partners with neuropilin 1 (Nrp1) to form a functional receptor for the vascular guidance molecule semaphorin 3d (Sema3d). Loss of Sema3d leads to improper patterning of the coronary veins, a phenotype recapitulated by endothelial loss of ErbB2. These findings have implications for possible cardiovascular side-effects of anti-ErbB2 therapies commonly used for cancer, and provide an example of integration at the molecular level of pathways involved in tissue growth and vascular patterning.
Date: 2016
References: Add references at CitEc
Citations:
Downloads: (external link)
https://www.nature.com/articles/ncomms12038 Abstract (text/html)
Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.
Export reference: BibTeX
RIS (EndNote, ProCite, RefMan)
HTML/Text
Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12038
Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/
DOI: 10.1038/ncomms12038
Access Statistics for this article
Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie
More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().