論文

査読有り 筆頭著者
2016年7月

In utero and lactational dioxin exposure induces Sema3b and Sema3g gene expression in the developing mouse brain

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
  • Eiki Kimura
  • ,
  • Toshihiro Endo
  • ,
  • Wataru Yoshioka
  • ,
  • Yunjie Ding
  • ,
  • Waka Ujita
  • ,
  • Masaki Kakeyama
  • ,
  • Chiharu Tohyama

476
2
開始ページ
108
終了ページ
113
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.bbrc.2016.05.048
出版者・発行元
ACADEMIC PRESS INC ELSEVIER SCIENCE

In the developing mammalian brain, neural network formation is regulated by complex signaling cascades. In utero and lactational dioxin exposure is known to induce higher brain function abnormalities and dendritic growth disruption in rodents. However, it is unclear whether perinatal dioxin exposure affects the expression of genes involved in neural network formation. Therefore, we investigated changes in gene expression in the brain regions of developing mice born to dams administered 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dose: 0, 0.6, or 3.0 mu g/kg) on gestational day 12.5. Quantitative RT-PCR showed that TCDD exposure induced Ahrr expression in the cerebral cortex, hippocampus, and olfactory bulb of 3-day-old mice. Gene microarray analysis indicated that the mRNA expression levels of Sema3b and Sema3g, which encode proteins that are known to control axonal projections, were elevated in the olfactory bulb of TCDD-exposed mice, and the induction of these genes was observed during a 2 week postnatal period. Increased Sema3g expression was also observed in the brain but not in the kidney, liver, lung, and spleen of TCDD-exposed neonatal mice. These results indicate that the Sema3b and Sema3g genes are sensitive to brain-specific induction by dioxin exposure, which may disrupt neural network formation in the mammalian nervous system, thereby leading to abnormal higher brain function in adulthood. (C) 2016 Elsevier Inc. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.bbrc.2016.05.048
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/27178212
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000378370300009&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.bbrc.2016.05.048
  • ISSN : 0006-291X
  • eISSN : 1090-2104
  • PubMed ID : 27178212
  • Web of Science ID : WOS:000378370300009

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