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糖原合成酶激酶-3β和雷帕霉素靶蛋白磷酸化介导弱磁场对成体神经干细胞增殖的可逆性调控。

GSK-3β and mTOR Phosphorylation Mediate the Reversible Regulation of Hypomagnetic Field on Adult Neural Stem Cell Proliferation.

作者信息

Ren Jie, Li Fulai, Shen Jianxun, Tian Lanxiang, Pan Yongxin

机构信息

Biogeomagnetism Group, Key Laboratory of Planetary Science and Frontier Technology, Institute of Geology and Geophysics, Chinese Academy of Sciences, Beijing, China.

College of Earth and Planetary Sciences, University of Chinese Academy of Sciences, Beijing, China.

出版信息

Eur J Neurosci. 2025 Jul;62(2):e70202. doi: 10.1111/ejn.70202.

Abstract

Exposure to hypomagnetic field (HMF) of < 5 μT has been demonstrated to impair cognitive behaviors in mammals by disrupting neurogenesis. This process could potentially be modulated by the protein phosphorylation of adult neural stem cells (aNSCs) that are highly sensitive to environmental changes. However, the effects of HMF on aNSCs protein phosphorylation remain unclear. Here, we found that HMF reversibly regulates the effects on aNSC proliferation by modulating protein phosphorylation in aNSCs. Specifically, HMF inhibits aNSCs proliferation by reducing glycogen synthase kinase 3β (GSK-3β) phosphorylation, and when aNSCs are returned from HMF to the geomagnetic field (rGMF), rGMF activates mammalian target of rapamycin (mTOR) phosphorylation to restore their proliferation. These findings not only advance our understanding of the molecular basis of HMF-induced biological effects but also illuminate potential therapeutic targets for maintaining neural homeostasis in extreme environments.

摘要

已证明暴露于小于5微特斯拉的低磁场(HMF)会通过破坏神经发生来损害哺乳动物的认知行为。这一过程可能会受到对环境变化高度敏感的成年神经干细胞(aNSCs)蛋白质磷酸化的调节。然而,HMF对aNSCs蛋白质磷酸化的影响仍不清楚。在这里,我们发现HMF通过调节aNSCs中的蛋白质磷酸化来可逆地调节对aNSC增殖的影响。具体而言,HMF通过降低糖原合酶激酶3β(GSK-3β)的磷酸化来抑制aNSCs的增殖,而当aNSCs从HMF回到地磁场(rGMF)时,rGMF会激活雷帕霉素哺乳动物靶标(mTOR)的磷酸化以恢复其增殖。这些发现不仅推进了我们对HMF诱导的生物学效应分子基础的理解,还为在极端环境中维持神经稳态阐明了潜在的治疗靶点。

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