演題番号 : P3-d10
柴田 雅祥 / Masayoshi Shibata:1 久米 伸恵 / Nobue Kume:1 大津 昌弘 / Masahiro Otsu:2 吉江 拓也 / Takuya Yoshie:1 上田 理沙 / Risa Ueda:1 大森 啓之 / Hiroyuki Omori:1 中山 孝 / Takashi Nakayama:3 鈴木 豊 / Yutaka Suzuki:4 近藤 靖 / Yasushi Kondo:4 井上 順雄 / Nobuo Inoue:1
1:首都大院・人間健康科学・フロンティアヘルスサイエンス / Dept Frontier Health Sci, Tokyo Metropolitan Univ Grad Sch of Human Health Sci, Tokyo 2:杏林大・医・化学 / Dept Chem, Kyorin Univ Sch of Med, Tokyo 3:横浜市立大・医・生化学 / Dept Biochem, Yokohama City Univ Sch of Med, Yokohama 4:田辺三菱製薬・先端医療研・再生医療 / Regene Med, Adv Med Res Lab, Mitsubishi Tanabe Pharma Co
Methylmercury (MeHg), a cause of Minamata disease, has been reported to act as a neurotoxic agent during brain development and to produce fetal Minamata disease, which is characterized by brain malformation and malfunction. We have reported that proliferation of neural stem cells (NSCs), prepared from mouse and monkey embryonic stem (ES) cells by the Neural Stem Sphere (NSS) method, is dose-dependently inhibited by MeHg. In this study, effects of MeHg on differentiation of monkey NSCs were investigated. When the NSCs were induced to differentiate into neurons in the presence of MeHg (from 100 nM to 3 μM), the cell number was dose-dependently decreased. In addition, the cells differentiating into neurons and the neurons differentiated from the NSCs were demonstrated to be more susceptive to MeHg than the proliferating NSCs. The effects of MeHg on the cells were supported by gene expression analysis using RT-PCR and immunofluorescent analysis. These results suggest that MeHg inhibits both proliferation and neuronal differentiation of the NSCs and that it consequently causes neurotoxic effects in the development of central nervous system.