Document Detail

Molecular identification of venous progenitors in the dorsal aorta reveals an aortic origin for the cardinal vein in mammals.
MedLine Citation:
PMID:  24550118     Owner:  NLM     Status:  MEDLINE    
Coordinated arterial-venous differentiation is crucial for vascular development and function. The origin of the cardinal vein (CV) in mammals is unknown, while conflicting theories have been reported in chick and zebrafish. Here, we provide the first molecular characterization of endothelial cells (ECs) expressing venous molecular markers, or venous-fated ECs, within the emergent dorsal aorta (DA). These ECs, expressing the venous molecular markers Coup-TFII and EphB4, cohabited the early DA with ECs expressing the arterial molecular markers ephrin B2, Notch and connexin 40. These mixed ECs in the early DA expressed either the arterial or venous molecular marker, but rarely both. Subsequently, the DA exhibited uniform arterial markers. Real-time imaging of mouse embryos revealed EC movement from the DA to the CV during the stage when venous-fated ECs occupied the DA. We analyzed mutants for EphB4, which encodes a receptor tyrosine kinase for the ephrin B2 ligand, as we hypothesized that ephrin B2/EphB4 signaling may mediate the repulsion of venous-fated ECs from the DA to the CV. Using an EC quantification approach, we discovered that venous-fated ECs increased in the DA and decreased in the CV in the mutants, whereas the rest of the ECs in each vessel were unaffected. This result suggests that the venous-fated ECs were retained in the DA and missing in the CV in the EphB4 mutant, and thus that ephrin B2/EphB4 signaling normally functions to clear venous-fated ECs from the DA to the CV by cell repulsion. Therefore, our cellular and molecular evidence suggests that the DA harbors venous progenitors that move to participate in CV formation, and that ephrin B2/EphB4 signaling regulates this aortic contribution to the mammalian CV.
Henrik Lindskog; Yung Hae Kim; Eric B Jelin; Yupeng Kong; Salvador Guevara-Gallardo; Tyson N Kim; Rong A Wang
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Development (Cambridge, England)     Volume:  141     ISSN:  1477-9129     ISO Abbreviation:  Development     Publication Date:  2014 Mar 
Date Detail:
Created Date:  2014-02-19     Completed Date:  2014-04-30     Revised Date:  2014-06-23    
Medline Journal Info:
Nlm Unique ID:  8701744     Medline TA:  Development     Country:  England    
Other Details:
Languages:  eng     Pagination:  1120-8     Citation Subset:  IM    
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MeSH Terms
Aorta / cytology*
Endothelial Cells / cytology,  metabolism
Mice, Transgenic
Neovascularization, Physiologic / physiology
Signal Transduction / physiology
Stem Cells / cytology*,  metabolism
Veins / cytology*
Grant Support
F32 HL097400/HL/NHLBI NIH HHS; R01 HL075033/HL/NHLBI NIH HHS; T32 HL007544/HL/NHLBI NIH HHS; T32 HL007544/HL/NHLBI NIH HHS; //Howard Hughes Medical Institute

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