Patent ductus arteriosus in mice with smooth muscle-specific Jag1 deletion.
Document Type
Article
Publication Date
2010
Keywords
Animals-Newborn, Calcium-Binding-Proteins, Cardiovascular-Agents, Cell-Differentiation, Ductus-Arteriosus-Patent, Embryo-Mammalian, Fluorescent-Antibody-Technique, Indomethacin, Intercellular-Signaling-Peptides-and-Proteins, Membrane-Proteins, Mice, Microscopy-Electron-Transmission, Muscle-Smooth-Vascular, Myocytes-Smooth-Muscle, Receptor-Notch1, Reverse-Transcriptase-Polymerase-Chain-Reaction
First Page
4191
Last Page
4199
JAX Source
Development 2010 Dec; 137(24):4191-9.
Abstract
The ductus arteriosus is an arterial vessel that shunts blood flow away from the lungs during fetal life, but normally occludes after birth to establish the adult circulation pattern. Failure of the ductus arteriosus to close after birth is termed patent ductus arteriosus and is one of the most common congenital heart defects. Mice with smooth muscle cell-specific deletion of Jag1, which encodes a Notch ligand, die postnatally from patent ductus arteriosus. These mice exhibit defects in contractile smooth muscle cell differentiation in the vascular wall of the ductus arteriosus and adjacent descending aorta. These defects arise through an inability to propagate the JAG1-Notch signal via lateral induction throughout the width of the vascular wall. Both heterotypic endothelial smooth muscle cell interactions and homotypic vascular smooth muscle cell interactions are required for normal patterning and differentiation of the ductus arteriosus and adjacent descending aorta. This new model for a common congenital heart defect provides novel insights into the genetic programs that underlie ductus arteriosus development and closure.
Recommended Citation
Feng X,
Krebs LT,
Gridley T.
Patent ductus arteriosus in mice with smooth muscle-specific Jag1 deletion. Development 2010 Dec; 137(24):4191-9.