Endothelial expression of the Notch ligand Jagged1 is required for vascular smooth muscle development
The Notch ligand Jagged1 (Jag1) is essential for vascular remodeling and has been linked to congenital heart disease in humans, but its precise role in various cell types of the cardiovascular system has not been extensively investigated. We show that endothelial-specific deletion of Jag1 results in...
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Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 105; no. 6; pp. 1955 - 1959 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
National Academy of Sciences
12.02.2008
National Acad Sciences |
Subjects | |
Online Access | Get full text |
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Summary: | The Notch ligand Jagged1 (Jag1) is essential for vascular remodeling and has been linked to congenital heart disease in humans, but its precise role in various cell types of the cardiovascular system has not been extensively investigated. We show that endothelial-specific deletion of Jag1 results in embryonic lethality and cardiovascular defects, recapitulating the Jag1 null phenotype. These embryos show striking deficits in vascular smooth muscle, whereas endothelial Notch activation and arterial-venous differentiation appear normal. Endothelial Jag1 mutant embryos are phenotypically distinct from embryos in which Notch signaling is inhibited in endothelium. Together, these results imply that the primary role of endothelial Jag1 is to potentiate the development of neighboring vascular smooth muscle. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Author contributions: F.A.H. and J.A.E. designed research; F.A.H. and M.M.L. performed research; W.S.P., K.M.L., and K.H.K. contributed new reagents/analytic tools; F.A.H. analyzed data; and F.A.H. and J.A.E. wrote the paper. Edited by Eric N. Olson, University of Texas Southwestern Medical Center, Dallas, TX, and approved December 18, 2007 |
ISSN: | 0027-8424 1091-6490 |
DOI: | 10.1073/pnas.0709663105 |