Asanuma Masato, Miyazaki Ikuko, Cadet Jean Lud
Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Kita-ku, Okayama, 700-8558, Japan.
Molecular Neuropsychiatry Section, Intramural Research Program, NIH/ NIDA, 21224, Baltimore, MD, U.S.A..
Neurotox Res. 2025 Jan 14;43(1):4. doi: 10.1007/s12640-024-00725-z.
To identify factors involved in methamphetamine (METH) neurotoxicity, we comprehensively searched for genes which were differentially expressed in mouse striatum after METH administration using differential display (DD) reverse transcription-PCR method and sequent single-strand conformation polymorphism analysis, and found two DD cDNA fragments later identified as mRNA of Nedd4 (neural precursor cell expressed developmentally downregulated 4) WW domain-binding protein 5 (N4WBP5), later named Nedd4 family-interacting protein 1 (Ndfip1). It is an adaptor protein for the binding between Nedd4 of ubiquitin ligase (E3) and target substrate protein for ubiquitination. Northern blot analysis confirmed drastic increases in Ndfip1 mRNA in the striatum after METH injections, and in situ hybridization histochemistry showed that the mRNA expression was increased in the hippocampus and cerebellum at 2 h-2 days, in the cerebral cortex and striatum at 18 h-2 days after single METH administration. The knockdown of Ndfip1 expression with Ndfip1 siRNA significantly aggravated METH-induced neurotoxicity in the cultured monoaminergic neuronal cells. These results suggest that drastic increases in Ndfip1 mRNA is compensatory reaction to protect neurons against METH-induced neurotoxicity.
为了确定与甲基苯丙胺(METH)神经毒性相关的因素,我们使用差异显示(DD)逆转录 - PCR方法及后续的单链构象多态性分析,全面搜索了METH给药后在小鼠纹状体中差异表达的基因,并发现了两个DD cDNA片段,后来鉴定为Nedd4(神经前体细胞表达发育下调基因4)WW结构域结合蛋白5(N4WBP5)的mRNA,后命名为Nedd4家族相互作用蛋白1(Ndfip1)。它是一种衔接蛋白,用于泛素连接酶(E3)的Nedd4与靶底物蛋白之间的结合以进行泛素化。Northern印迹分析证实,METH注射后纹状体中Ndfip1 mRNA急剧增加,原位杂交组织化学显示,单次给予METH后2小时至2天,海马体和小脑中mRNA表达增加,18小时至2天在大脑皮质和纹状体中mRNA表达增加。用Ndfip1 siRNA敲低Ndfip1表达显著加重了培养的单胺能神经元细胞中METH诱导的神经毒性。这些结果表明,Ndfip1 mRNA的急剧增加是一种保护神经元免受METH诱导的神经毒性的代偿反应。