Branchial arch artery formation and apoptosis during cardiogenesis in the Ts65Dn mouse model for Down syndrome
Ts65Dn is the mouse model most widely used in Down syndrome (DS) research. In this model, triplication of the distal portion of mouse chromosome 16 (MMU16), which contains orthologs to genes on human chromosome 21, results in cardiac defects reminiscent of DS congenital heart disease. In our study, embryonic cardiovascular development was examined at stages critical for septation in order to investigate the spatial and temporal origins of cardiovascular deformities, such as right aortic arch and septal defects, previously identified in neonatal Ts65Dn mice. Analysis of the branchial arch arteries, which are remodeled into the great thoracic vessels, demonstrates developmental malformations in 10.5 day post coitum Ts65Dn embryos. During remodeling of the endocardial cushions, the amount of apoptosis in the atrioventricular region and the outflow tract was reduced in Ts65Dn compared to euploid embryos. These findings suggest developmental origins for the cardiac anomalies seen in Ts65Dn newborn mice and demonstrate the etiology of the vascular malformations and septal defects.
Franklin and Marshall College Archives, Undergraduate Honors Thesis 2007
- F&M Theses Collection