Endothelial expression of the Notch ligand Jagged1 is required for vascular smooth muscle development

被引：250

作者：

High, Frances A. ^{[1
,2
]}

Lu, Min Min ^{[1
,2
]}

Pear, Warren S. ^{[3
,4
]}

Loomes, Kathleen M. ^{[7
,8
]}

Kaestner, Klaus H. ^{[5
,6
]}

Epstein, Jonathan A. ^{[1
,2
]}

机构：

[1] Univ Penn, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA

[2] Univ Penn, Cardiovasc Inst, Philadelphia, PA 19104 USA

[3] Univ Penn, Inst Med & Engn, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA

[4] Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA

[5] Univ Penn, Dept Genet, Philadelphia, PA 19104 USA

[6] Univ Penn, Inst Diabet Obes & Metab, Philadelphia, PA 19104 USA

[7] Childrens Hosp, Div Gastroenterol Hepatol & Nutr, Philadelphia, PA 19104 USA

[8] Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2008年 / 105卷 / 06期

关键词：

D O I：

10.1073/pnas.0709663105

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页码：1955 / 1959

页数：5

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