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Analysis of Neural Crest Migration and Differentiation by Cross-species Transplantation
Published on: February 7, 2012
PlexinA2 and semaphorin signaling during cardiac neural crest development
1Department of Medicine, University of Pennsylvania, Philadelphia 19104, USA.
Abstract:
Classic studies using avian model systems have demonstrated that cardiac neural crest cells are required for proper development of the cardiovascular system. Environmental influences that perturb neural crest development cause congenital heart defects in laboratory animals and in man. However, little progress has been made in determining molecular programs specifically regulating cardiac neural crest migration and function. Only recently have complex transgenic tools become available that confirm the presence of cardiac neural crest cells in the mammalian heart. These studies have relied upon the use of transgenic mouse lines and fate-mapping studies using Cre recombinase and neural crest-specific promoters. In this study, we use these techniques to demonstrate that PlexinA2 is expressed by migrating and postmigratory cardiac neural crest cells in the mouse. Plexins function as co-receptors for semaphorin signaling molecules and mediate axon pathfinding in the central nervous system. We demonstrate that PlexinA2-expressing cardiac neural crest cells are patterned abnormally in several mutant mouse lines with congenital heart disease including those lacking the secreted signaling molecule Semaphorin 3C. These data suggest a parallel between the function of semaphorin signaling in the central nervous system and in the patterning of cardiac neural crest in the periphery.
Insights
PlexinA2 is crucial for cardiac neural crest cell development and function. Its abnormal patterning in congenital heart disease models highlights the role of semaphorin signaling in cardiovascular development.
Area of Science:
- Developmental biology
- Cardiovascular science
- Neuroscience
Background:
- Cardiac neural crest cells are essential for cardiovascular development.
- Environmental factors impacting neural crest development can lead to congenital heart defects.
- Molecular mechanisms regulating cardiac neural crest cell migration and function are not well understood.
Purpose of the Study:
- To investigate the role of PlexinA2 in mammalian cardiac neural crest cell development.
- To determine the involvement of semaphorin signaling in cardiac neural crest cell patterning.
- To explore the link between PlexinA2 expression and congenital heart disease.
Main Methods:
- Utilized transgenic mouse lines and Cre-lox fate-mapping techniques.
- Examined PlexinA2 expression in migrating and postmigratory cardiac neural crest cells.
- Analyzed cardiac neural crest cell patterning in congenital heart disease mutant mouse models, including those deficient in Semaphorin 3C.
Main Results:
- PlexinA2 is expressed in migrating and postmigratory cardiac neural crest cells in mice.
- Abnormal patterning of PlexinA2-expressing cardiac neural crest cells was observed in congenital heart disease models.
- These defects were noted in mice lacking Semaphorin 3C, a key semaphorin signaling molecule.
Conclusions:
- PlexinA2 plays a significant role in cardiac neural crest cell development and patterning.
- Semaphorin signaling, mediated by PlexinA2, is important for cardiovascular development.
- This suggests a conserved role for semaphorin signaling in both the central nervous system and peripheral cardiovascular development.
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