Literature DB >> 18937363

Wnt signaling in caudal dysgenesis and diabetic embryopathy.

Gabriela Pavlinkova1, J Michael Salbaum, Claudia Kappen.   

Abstract

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. Copyright 2008 Wiley-Liss, Inc.

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Year:  2008        PMID: 18937363      PMCID: PMC2963627          DOI: 10.1002/bdra.20495

Source DB:  PubMed          Journal:  Birth Defects Res A Clin Mol Teratol        ISSN: 1542-0752


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9.  Superoxide Dismutase 1 In Vivo Ameliorates Maternal Diabetes Mellitus-Induced Apoptosis and Heart Defects Through Restoration of Impaired Wnt Signaling.

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