Wnt signaling in caudal dysgenesis and diabetic embryopathy
Article first published online: 20 OCT 2008
Copyright © 2008 Wiley-Liss, Inc.
Birth Defects Research Part A: Clinical and Molecular Teratology
Special Issue: Remembering Marcy Speer
Volume 82, Issue 10, pages 710–719, October 2008
How to Cite
Pavlinkova, G., Salbaum, J. M. and Kappen, C. (2008), Wnt signaling in caudal dysgenesis and diabetic embryopathy. Birth Defects Research Part A: Clinical and Molecular Teratology, 82: 710–719. doi: 10.1002/bdra.20495
- Issue published online: 20 OCT 2008
- Article first published online: 20 OCT 2008
- Manuscript Accepted: 23 JUN 2008
- Manuscript Revised: 6 JUN 2008
- Manuscript Received: 25 APR 2008
- NIH. Grant Numbers: RO1-HD37804, RO1-HD37804-S1
- maternal diabetes;
- caudal dysgenesis;
- neural tube defect;
- Wnt pathway;
- expression studies;
- developmental programs;
- mouse model;
- transcriptional regulation
Congenital defects are a major complication of diabetic pregnancy, and the leading cause of infant death in the first year of life. Caudal dysgenesis, occurring up to 200-fold more frequently in children born to diabetic mothers, is a hallmark of diabetic pregnancy. Given that there is also an at least threefold higher risk for heart defects and NTDs, it is important to identify the underlying molecular mechanisms for aberrant embryonic development.
We have investigated gene expression in a transgenic mouse model of caudal dysgenesis, and in a pharmacological model using situ hybridization and quantitative real-time PCR.
We identified altered expression of several molecules that control developmental processes and embryonic growth.
The results from our models point towards major implication of altered Wnt signaling in the pathogenesis of developmental anomalies associated with embryonic exposure to maternal diabetes. Birth Defects Research (Part A) 82:710–719, 2008. © 2008 Wiley-Liss, Inc.