Journal
BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
Volume 82, Issue 10, Pages 710-719Publisher
WILEY-BLACKWELL
DOI: 10.1002/bdra.20495
Keywords
maternal diabetes; caudal dysgenesis; neural tube defect; Wnt pathway; expression studies; developmental programs; midgestation; mouse model; transgenic; transcriptional regulation
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Funding
- NIH [RO1-HD37804, RO1-HD37804-S1]
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R01HD037804] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR018788] Funding Source: NIH RePORTER
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BACKGROUND: 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. METHODS: 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. RESULTS: We identified altered expression of several molecules that control developmental processes and embryonic growth. CONCLUSIONS: 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. (C) 2008 Wiley-Liss, Inc.
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