Cardiovascular Development and Survival During Gestation in the Ts65Dn Mouse Model for Down Syndrome

被引：13

作者：

Lorandeau, Candice G. ^{[1
]}

Hakkinen, Lauren A. ^{[1
]}

Moore, Clara S. ^{[1
]}

机构：

[1] Franklin & Marshall Coll, Dept Biol, Lancaster, PA 17604 USA

来源：

ANATOMICAL RECORD-ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY | 2011年 / 294卷 / 01期

关键词：

Down syndrome model; cardiovascular development; prenatal survival; pharyngeal arch arteries; 5TH AORTIC-ARCH; CARDIAC ANOMALIES; FETAL LOSS; CHROMOSOME; PHENOTYPES; FETUSES; HUMAN-CHROMOSOME-21; ABNORMALITIES; MALFORMATIONS; REGION;

D O I：

10.1002/ar.21301

中图分类号：

R602 [外科病理学、解剖学]; R32 [人体形态学];

学科分类号：

100101 ;

摘要：

The Ts65Dn mouse model for Down syndrome (DS) exhibits many phenotypes seen in human DS. Previous research has revealed a reduced rate of transmission of the T65Dn marker chromosome in neonates. To analyze potential fetal loss, litters from trisomic females at 10.5dpc through 14.5dpc were genotyped. No significant differences from the expected Mendelian ratio were found in transmission of T65Dn at any stage. Cardiovascular defects found in trisomic neonates are associated with formation of pharyngeal arch arteries. Vessel tracing was used to identify anomalies in 10.5dpc, 11.5dpc, and 13.5dpc embryos. Comparison of trisomic versus euploid embryos injected with India ink revealed delay and abnormality in cardiovascular development in trisomic embryos at each stage. Through the analysis of transmission rate and cardiovascular development in embryonic mice, we learn more about prenatal mortality and the origins of cardiac abnormality in the Ts65Dn mice to assist in understanding cardiovascular malformation associated with DS. Anat Rec, 294:93-101, 2011. (C) 2010 Wiley-Liss, Inc.

引用

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页码：93 / 101

页数：9

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