Identification of Genes Differentially Expressed in Mouse Fetuses from Streptozotocin-induced Diabetic Pregnancy by cDNA Subtraction

• SATO Nanako

  Department of Genetics, Research Institute of Environmental Medicine, Nagoya University Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine

• SUGIMURA Yoshihisa

  Department of Genetics, Research Institute of Environmental Medicine, Nagoya University Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine

• HAYASHI Yoshitaka

  Department of Genetics, Research Institute of Environmental Medicine, Nagoya University

• MURASE Takashi

  Department of Genetics, Research Institute of Environmental Medicine, Nagoya University

• KANOU Yasuhiko

  Department of Genetics, Research Institute of Environmental Medicine, Nagoya University Futuristic Environmental Simulation Center, Research Institute of Environmental Medicine, Nagoya University

• KIKKAWA Fumitaka

  Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine

• MURATA Yoshiharu

  Department of Genetics, Research Institute of Environmental Medicine, Nagoya University

抄録

Epidemiological studies have shown that the risks of fetal malformation such as neural tube defects increase in diabetic pregnancy. To explore the mechanism of fetal malformation induced by diabetes, cDNA subtraction using mouse embryos (E9.5) of diabetic dams and those of controls was performed to identify differentially expressed genes. The expression level of genes identified by cDNA subtraction was further verified by quantitative RT-PCR using E8.5 embryos, and differential expression of 4 genes, Brcc3, Commd3, Ddx1, and SET was confirmed. We also analyzed the expression level of neural tube defect-related genes, and found that Folbp1, EphrinA5 and Sox10 were differentially expressed. Altered expression of these genes mostly persisted throughout the later stages of the development (E10.5-14.5). Hierarchical clustering analysis showed correlation between expression levels of these genes, suggesting that these genes cooperatively play a role in embryonic development. Our results suggest that an altered gene expression profile in embryos underlies the development of congenital malformation in diabetic pregnancies.<br>

収録刊行物

• Endocrine Journal

  Endocrine Journal 55 (2), 317-323, 2008

  一般社団法人 日本内分泌学会

キーワード

• Congenital malformation
• Neural tube defect
• cDNA subtraction
• Gene expression profile
• Embryonic development

詳細情報

• CRID: 1390001206298871552
• NII論文ID: 10021265571
• NII論文ID: 130004443395
• NII書誌ID: AA10901436
• DOI: 10.1507/endocrj.k07-117
• ISSN: 13484540
• ISSN: 09188959
• Web Site: http://www.jstage.jst.go.jp/article/endocrj/55/2/55_K07-117/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2008234285
• 本文言語コード: en
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