Identification of genes differentially expressed in mouse fetuses from streptozotocin-induced diabetic pregnancy by

Nanako Sato1, Yoshihisa Sugimura, Yoshitaka Hayashi

  • 1Department of Genetics, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan.

Endocrine Journal
|March 8, 2008
PubMed

Insights

Diabetic pregnancy increases fetal malformation risks. This study identified altered gene expression in mouse embryos, revealing potential mechanisms for congenital malformations in diabetic pregnancies.

Area of Science:

  • Developmental biology
  • Genetics
  • Reproductive medicine

Background:

  • Diabetic pregnancy is linked to increased fetal malformations, including neural tube defects.
  • The underlying molecular mechanisms remain incompletely understood.

Purpose of the Study:

  • To identify differentially expressed genes in mouse embryos from diabetic dams.
  • To elucidate the molecular basis of congenital malformations in diabetic pregnancies.

Main Methods:

  • Utilized cDNA subtraction to identify genes with altered expression in mouse embryos (E9.5) from diabetic versus control dams.
  • Confirmed differential gene expression using quantitative RT-PCR (E8.5) and analyzed neural tube defect-related genes.
  • Assessed gene expression persistence (E10.5-14.5) and performed hierarchical clustering analysis.

Main Results:

  • Identified differential expression of four genes: Brcc3, Commd3, Ddx1, and SET.
  • Found altered expression of neural tube defect-related genes: Folbp1, EphrinA5, and Sox10.
  • Observed persistent altered expression and correlated expression patterns, suggesting cooperative roles in embryonic development.

Conclusions:

  • Altered gene expression profiles in embryos are implicated in congenital malformations associated with diabetic pregnancies.
  • Specific genes identified may serve as targets for understanding and potentially preventing these malformations.

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