Publication List Japanese

2017/07/01
化学工業 Vol.68No.7 ゼブラフィッシュ創薬とInternet of Zebrafish(IoZ)

2017/05/22
月刊ファームステージ Vol.17 No.2 ゼブラフィッシュ創薬とフェノミクス薬理学

2017/03/31
NEW薬理学 改訂第7版 プロテオーム創薬

2016/10/19
三重大学春秋会会報 第39号 ゼブラフィッシュ創薬への道程 

2016/10/07
理系マイナビ special interview

》バルプロ酸の発達神経毒性に関するシステムズ薬理学

                     
2015/03/18

バルプロ酸の発達神経毒性に関するシステムズ薬理学

村上宗一郎1、西村有平1,2,3,4,5、笹川翔太1、芦川芳史1、弓削瑞葵1、有吉美稚子1、川瀬玲子1、田中利男1,2,3,4,5

1三重大学大学院医学系研究科薬理ゲノミクス(三重大・院・医・薬理ゲノミクス)
2三重大・院・医・システムズ薬理学
3三重大・メディカルゼブラフィッシュ研究センター
4三重大・生命科学研セ・バイオインフォ
5三重大・新産業創成研究拠点

It is well known that exposure to valproic acid (VPA) during developmental period may cause various neuropsychiatric disorders. However, the detailed mechanism has been unknown. To elucidate the molecular mechanism, we exposed VPA to fertilized eggs of zebrafish and analyzed the gene expression variations comprehensively using DNA microarray comparing with publicly available transcriptome data analyzing the effect of VPA in developmental stages. As a result, we discovered that the expression of epc2 was significantly decreased by VPA exposure at developmental stages in both zebrafish and mouse. EPC2 is one of the polycomb genes and related to 2q23.1 microdeletion syndrome characterized by psychomotor retardation, seizure, and stereotypic repetitive behavior. Then, we knocked out epc2 gene in zebrafish using TALEN to analyze the functional role of epc2 downregulation by VPA exposure. We were able to identify several genes dysregulated in common between zebrafish exposed to VPA and zebrafish with epc2 knockout, suggesting that epc2 may be involved at least partly in developmental neurotoxicity of VPA.

関連リンク

第88回日本薬理学会年会