Fetal exposure to diesel exhaust affects X-chromosome inactivation factor expression in mice

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  • Kumamoto Takayuki
    School of Pharmaceutical Science, Ohu University Faculty of Pharmaceutical Science, Tokyo University of Science Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology (JST)
  • Tsukue Naomi
    Faculty of Pharmaceutical Science, Tokyo University of Science Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology (JST)
  • Takano Hirohisa
    Environmental Health Sciences Division, National Institute for Environmental Studies Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology (JST)
  • Takeda Ken
    Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology (JST) Faculty of Pharmaceutical Science, Tokyo University of Science
  • Oshio Shigeru
    Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology (JST) Faculty of Pharmaceutical Science, Tokyo University of Science School of Pharmaceutical Science, Ohu University

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Several studies have shown effects of diesel exhaust (DE) on the central nervous system, but the mechanism is unclear. Fetal mice were exposed to whole DE (contains gases and particles) in an inhalation chamber, and cerebrum gene expression changes were examined by gene assay (microarray and quantitative real-time PCR). By microarray, upregulation of Xist, B-raf and Drwms2 were detected. Especially, mRNA expression of Xist was increased in a concentration-dependent manner in male and female mice. Xist (X-inactive specific transcript) is a major effector of the X-inactivation process, and X-linked genes are highly expressed in brain tissue and consistent with a role in brain developments. By quantitative real-time PCR, Tsix (crucial noncoding antisense partner of Xist) and other X-linked genes (Mecp2, Hprt1, and Sts) were examined; Tsix was upregulated, and other X-linked genes were unaffected in the male and female mice. Our findings suggest that exposure to DE increases Xist and Tsix gene expression in utero without influencing X-linked gene expression. An examination of Xist gene expression changes may provide an important biomarker for DE-induced effects. The possibility of avoiding X-chromosome inactivation (XCI) mechanisms by minimizing exposure to DE is expected.

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