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Genome Informatics, Proteomics, and Systems Biology

開催日 2014/9/11
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

Genomic responses in mouse models greatly mimic human inflammatory diseases: In defense of mouse models for studying human disorders

  • P1-389
  • 高雄 啓三 / Keizo Takao:1 宮川 剛 / Tsuyoshi Miyakawa:1,2 
  • 1:自然科学研究機構 生理学研究所 / National Institute for Physiological Sciences 2:藤田保健衛生大学 総合医科学研究所 / Fujita Health Univ. Toyoake, Japan 

The use of mice as animal models of human disorders has long been considered essential for elucidating the underlying mechanisms of disease, as well as for translational research from bench to bedside. However, the role of mouse models in biomedical research was recently challenged by a report that genomic responses in mouse models poorly mimic human inflammatory diseases (Seok J et al., Proc Natl Acad Sci USA, 2013). Here we re-evaluated the same gene expression datasets used in the previous study by focusing on genes whose expression levels were significantly changed in both humans and mice. Contrary to the previous findings, the gene expression levels in the mouse models showed extraordinary significant correlations with those of the human conditions (Spearman's rank correlation coefficient: between 0.43 and 0.68; the percentage of the genes changed in the same direction: between 77 and 93; P = 6.5 x 10-11 - 1.2 x 10-35). Moreover, meta-analysis of those datasets revealed a number of pathways/biogroups commonly regulated by multiple conditions in humans and mice. These findings demonstrate that gene expression patterns in mouse models closely recapitulate those in human inflammatory conditions and strongly argue for the utility of mice as animal models of human disorders.

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