Zinc Deficiency Decreases Neurite Extension via CRMP2 Signal Pathway.

IF 17.7 1区化学 Q1 CHEMISTRY, MULTIDISCIPLINARY Accounts of Chemical Research Pub Date : 2024-04-05 DOI:10.1248/bpb.b24-00019

H. Kurita, Misa Ueda, Miyu Kimura, Ayu Okuda, Kazuki Ohuchi, Isao Hozumi, Masatoshi Inden

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Abstract

Previous reports indicated that zinc deficiency could increase the risk of infectious diseases and developmental retardation in children. In experimental study, it has been reported that zinc deficiency during the embryonic period inhibited fetal growth, and disturbed neural differentiation and higher brain function later in adulthood. Although it has been suggested that zinc deficiency during development can have significant effects on neuronal differentiation and maturation, the molecular mechanisms of the effects of low zinc on neuronal differentiation during development have not been elucidated in detail. This study was performed to determine the effects of low zinc status on neurite outgrowth and collapsin response mediator protein 2 (CRMP2) signal pathway. Low zinc suppressed neurite outgrowth, and caused increase levels of phosphorylated CRMP2 (pCRMP2) relative to CRMP2, and decrease levels of phosphorylated glycogen synthase kinase 3β (pGSK3β) relative to GSK3β in human neuroblastoma cell line (SH-SY5Y) cells on days 1, 2, and 3 of neuronal differentiation induction. Neurite outgrowth inhibited by low zinc was restored by treatment with the GSK3β inhibitor CHIR99021. These results suggested that low zinc causes neurite outgrowth inhibition via phosphorylation of CRMP2 by GSK3β. In conclusion, this study is the first to demonstrate that CRMP signaling is involved in the suppression of neurite outgrowth by low zinc.

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缺锌会通过 CRMP2 信号通路减少神经元延伸

以往的报告显示，缺锌会增加儿童患传染病和发育迟缓的风险。在实验研究中，有报道称胚胎时期缺锌会抑制胎儿的生长，并干扰成年后的神经分化和大脑高级功能。虽然有研究认为发育期缺锌会对神经元的分化和成熟产生显著影响，但低锌对发育期神经元分化影响的分子机制尚未得到详细阐明。本研究旨在确定低锌状态对神经元突起生长和塌缩素反应介导蛋白2（CRMP2）信号通路的影响。在诱导神经元分化的第1、2和3天，低锌抑制了人神经母细胞瘤细胞株（SH-SY5Y）的神经元生长，并导致磷酸化CRMP2（pCRMP2）水平相对于CRMP2升高，磷酸化糖原合酶激酶3β（pGSK3β）水平相对于GSK3β降低。用 GSK3β 抑制剂 CHIR99021 处理后，低锌抑制的神经元生长得到恢复。这些结果表明，低锌通过 GSK3β 磷酸化 CRMP2 导致神经元生长受抑制。总之，本研究首次证明 CRMP 信号转导参与了低锌对神经元生长的抑制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Accounts of Chemical Research 化学-化学综合

CiteScore

31.40

自引率

1.10%

发文量

312

审稿时长

2 months

期刊介绍： Accounts of Chemical Research presents short, concise and critical articles offering easy-to-read overviews of basic research and applications in all areas of chemistry and biochemistry. These short reviews focus on research from the author’s own laboratory and are designed to teach the reader about a research project. In addition, Accounts of Chemical Research publishes commentaries that give an informed opinion on a current research problem. Special Issues online are devoted to a single topic of unusual activity and significance. Accounts of Chemical Research replaces the traditional article abstract with an article "Conspectus." These entries synopsize the research affording the reader a closer look at the content and significance of an article. Through this provision of a more detailed description of the article contents, the Conspectus enhances the article's discoverability by search engines and the exposure for the research.

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