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Wnt signaling in caudal dysgenesis and diabetic embryopathy

Authors

  • Gabriela Pavlinkova,

    1. Department of Pediatrics, University of Nebraska Medical Center, Omaha, Nebraska
    2. Department of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, Nebraska
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  • J. Michael Salbaum,

    1. Department of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, Nebraska
    2. Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, Nebraska
    3. Department of Regulation of Gene Expression, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, Louisiana
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  • Claudia Kappen

    Corresponding author
    1. Department of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, Nebraska
    2. Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, Nebraska
    3. Department of Maternal Biology, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, Louisiana
    • Pennington Biomedical Research Center/Louisiana State University, 6400 Perkins Rd., Baton Rouge, LA 70808
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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. Birth Defects Research (Part A) 82:710–719, 2008. © 2008 Wiley-Liss, Inc.

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