Cell Proliferation and Apoptosis in Heart of Trisomy 16 in Mice.
- Author:
Eun Jung BAE
1
;
Yong Soo YUN
;
Jung Sun KIM
;
Jeong Wook SEO
Author Information
1. Department of Pediatrics, Seoul National University College of Medicine and Heart Research Institute , Seoul National University Medical Research Center, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Trisomy 16 mouse;
Endocardial cushion;
Atrioventricular septal defect;
Cell proliferation;
apoptosis
- MeSH:
Animals;
Apoptosis*;
Cell Proliferation*;
Down Syndrome;
Embryonic Structures;
Endocardial Cushions;
Heart*;
In Situ Nick-End Labeling;
Mice*;
Models, Animal;
Morphogenesis;
Muscle Cells;
Proliferating Cell Nuclear Antigen;
Trisomy*
- From:Journal of the Korean Pediatric Society
1999;42(5):621-630
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Although abnormal developments of cushion and atrioventricular septum have been suggested, the exact mechanism for the development of atrioventricular septal defect is not well known. We aimed to identify the role of cell proliferation and apoptosis on cardiac morphogenesis in trisomy 16 mice(an animal model for Down's syndrome in human). METHODS: We examined the difference in cardiac masses and structures of trisomy 16 mice and normal control mice at stages of embryonal day 11, day 14 and day 16, when the endocardial cushion grows rapidly. We prepared cardiac section slides with PCNA and TUNEL staining and measured the amount, location of cell proliferation and apoptosis with computerized image analysis system. RESULTS: Atrioventricular septal defects were evident at day 14 and day 16 trisomy embryos. The ventricle areas were smaller in trisomy mice especially at day 14 embryos(P=0.04). And the cell proliferation rates were lower in trisomy mice along these periods. The rate of apoptosis was lower in trisomy embryo than control at both ventricular myocytes and interventricular septum, but characteristically apoptotic bodies were condensed at endocardial cushion area in trisomy 16 embryo. CONCLUSION: The developmental problems of atrioventricular septal defect of trisomy 16 mice resulted from myocardial hypoplasia and late localized apoptosis at cushion area, and these changes may play an important role in ventricular remodelling of atrioventricular septal defect.
