Sox17 is indispensable for acquisition and maintenance of arterial identity
Monica Corada,
Fabrizio Orsenigo,
Marco Francesco Morini,
Mara Elena Pitulescu,
Ganesh Bhat,
Daniel Nyqvist,
Ferruccio Breviario,
Valentina Conti,
Anais Briot,
M. Luisa Iruela-Arispe,
Ralf H. Adams and
Elisabetta Dejana ()
Additional contact information
Monica Corada: FIRC Institute of Molecular Oncology (IFOM)
Fabrizio Orsenigo: FIRC Institute of Molecular Oncology (IFOM)
Marco Francesco Morini: FIRC Institute of Molecular Oncology (IFOM)
Mara Elena Pitulescu: Max Planck Institute for Molecular Biomedicine and Faculty of Medicine, University of Münster
Ganesh Bhat: FIRC Institute of Molecular Oncology (IFOM)
Daniel Nyqvist: Karolinska Institutet
Ferruccio Breviario: FIRC Institute of Molecular Oncology (IFOM)
Valentina Conti: Stem Cells and Gene Therapy DIBIT H San Raffaele
Anais Briot: Cell and Developmental Biology, University of California
M. Luisa Iruela-Arispe: Cell and Developmental Biology, University of California
Ralf H. Adams: Max Planck Institute for Molecular Biomedicine and Faculty of Medicine, University of Münster
Elisabetta Dejana: FIRC Institute of Molecular Oncology (IFOM)
Nature Communications, 2013, vol. 4, issue 1, 1-14
Abstract:
Abstract The functional diversity of the arterial and venous endothelia is regulated through a complex system of signalling pathways and downstream transcription factors. Here we report that the transcription factor Sox17, which is known as a regulator of endoderm and hemopoietic differentiation, is selectively expressed in arteries, and not in veins, in the mouse embryo and in mouse postnatal retina and adult. Endothelial cell-specific inactivation of Sox17 in the mouse embryo is accompanied by a lack of arterial differentiation and vascular remodelling that results in embryo death in utero. In mouse postnatal retina, abrogation of Sox17 expression in endothelial cells leads to strong vascular hypersprouting, loss of arterial identity and large arteriovenous malformations. Mechanistically, Sox17 acts upstream of the Notch system and downstream of the canonical Wnt system. These data introduce Sox17 as a component of the complex signalling network that orchestrates arterial/venous specification.
Date: 2013
References: Add references at CitEc
Citations: View citations in EconPapers (6)
Downloads: (external link)
https://www.nature.com/articles/ncomms3609 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:4:y:2013:i:1:d:10.1038_ncomms3609
Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/
DOI: 10.1038/ncomms3609
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 ().