Suppr超能文献

谷氨酸转运体对人诱导多能干细胞源性神经细胞兴奋性毒性的神经保护作用。

Neuroprotective Potential of L-Glutamate Transporters in Human Induced Pluripotent Stem Cell-Derived Neural Cells against Excitotoxicity.

机构信息

Laboratory of Neuropharmacology, Division of Pharmacology, National Institute of Health Sciences, 3-25-26 Tonomachi, Kawasaki-ku, Kawasaki-city, Kanagawa 210-9501, Japan.

Department of Electronics, Graduate School of Engineering, Tohoku Institute of Technology, Miyagi 982-8577, Japan.

出版信息

Int J Mol Sci. 2023 Aug 9;24(16):12605. doi: 10.3390/ijms241612605.

Abstract

Human induced pluripotent stem cell (hiPSC)-derived neural cells have started to be used in safety/toxicity tests at the preclinical stage of drug development. As previously reported, hiPSC-derived neurons exhibit greater tolerance to excitotoxicity than those of primary cultures of rodent neurons; however, the underlying mechanisms remain unknown. We here investigated the functions of L-glutamate (L-Glu) transporters, the most important machinery to maintain low extracellular L-Glu concentrations, in hiPSC-derived neural cells. We also clarified the contribution of respective L-Glu transporter subtypes. At 63 days in vitro (DIV), we detected neuronal circuit functions in hiPSC-derived neural cells by a microelectrode array system (MEA). At 63 DIV, exposure to 100 μM L-Glu for 24 h did not affect the viability of neural cells. 100 µM L-Glu in the medium decreased to almost 0 μM in 60 min. Pharmacological inhibition of excitatory amino acid transporter 1 (EAAT1) and EAAT2 suppressed almost 100% of L-Glu decrease. In the presence of this inhibitor, 100 μM L-Glu dramatically decreased cell viability. These results suggest that in hiPSC-derived neural cells, EAAT1 and EAAT2 are the predominant L-Glu transporters, and their uptake potentials are the reasons for the tolerance of hiPSC-derived neurons to excitotoxicity.

摘要

人诱导多能干细胞(hiPSC)衍生的神经细胞已开始在药物开发的临床前阶段用于安全性/毒性测试。如前所述,hiPSC 衍生的神经元对兴奋毒性的耐受性高于鼠神经元原代培养物;然而,其潜在机制尚不清楚。我们在此研究了维持细胞外 L-谷氨酸(L-Glu)浓度较低的最重要机制——L-Glu 转运体在 hiPSC 衍生的神经细胞中的功能。我们还阐明了各自 L-Glu 转运体亚型的贡献。在体外 63 天(DIV)时,我们通过微电极阵列系统(MEA)检测 hiPSC 衍生的神经细胞中的神经元回路功能。在 63 DIV 时,用 100 μM L-Glu 处理 24 h 不会影响神经细胞的活力。在 60 分钟内,培养基中的 100 μM L-Glu 减少到几乎为 0 μM。兴奋性氨基酸转运蛋白 1(EAAT1)和 EAAT2 的药理学抑制几乎抑制了 100%的 L-Glu 减少。在抑制剂存在的情况下,100 μM L-Glu 显著降低了细胞活力。这些结果表明,在 hiPSC 衍生的神经细胞中,EAAT1 和 EAAT2 是主要的 L-Glu 转运体,其摄取潜力是 hiPSC 衍生的神经元对兴奋毒性具有耐受性的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29fe/10454411/d3af20f51c8a/ijms-24-12605-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验