Stanniocalcin 2通过激活AKT通路促进小鼠脑室下区神经干/祖细胞的神经元分化

Stem cells and development Pub Date : 2024-10-01 Epub Date: 2024-08-09 DOI:10.1089/scd.2024.0094
Zhenyu Guo, Hanyue Zhang, Xinbate Jingele, Jing Yan, Xinxiang Wang, Yingxi Liu, Tingqin Huang, Chongxiao Liu
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引用次数: 0

摘要

神经干细胞/祖细胞(NSPCs)终生存在于哺乳动物的室下区,对各种病理生理刺激做出反应,并在中枢神经系统修复中发挥着至关重要的作用。尽管已有大量研究阐明了斯坦尼钙素 2(STC2)在细胞分化过程中的调控作用,但人们对其在 NSPCs 分化过程中的具体功能仍知之甚少。阐明 STC2 在 NSPCs 中的作用对于设计新策略以提高损伤后脑再生的内在潜力至关重要。我们的研究揭示了 STC2 在 C57BL/6N 小鼠室下区(SVZ)衍生的 NSPCs 中的表达。在培养的SVZ衍生NSPCs中,STC2处理可显著增加Tuj1和DCX阳性细胞的数量。此外,将 STC2 注入侧脑室可促进 NSPCs 的神经元分化和向嗅球的迁移。相反,STC2敲除则会产生相反的效果。进一步的研究表明,STC2 处理会增强培养的 NSPCs 中 AKT 的磷酸化,而抑制 STC2 则会阻碍 AKT 的激活。值得注意的是,AKT抑制剂GSK690693阻断了STC2诱导的神经元分化,而AKT激活剂SC79逆转了STC2敲除对神经元分化的影响。我们的研究结果表明,提高SVC2在SVZ衍生NSPCs中的表达可促进神经元分化,而AKT调控可能是STC2信号传导的一个关键细胞内靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Stanniocalcin 2 Promotes Neuronal Differentiation in Neural Stem/Progenitor Cells of the Mouse Subventricular Zone Through Activation of AKT Pathway.

Neural stem/progenitor cells (NSPCs) persist in the mammalian subventricular zone (SVZ) throughout life, responding to various pathophysiological stimuli and playing a crucial role in central nervous system repair. Although numerous studies have elucidated the role of stanniocalcin 2 (STC2) in regulating cell differentiation processes, its specific function in NSPCs differentiation remains poorly understood. Clarifying the role of STC2 in NSPCs is essential for devising novel strategies to enhance the intrinsic potential for brain regeneration postinjury. Our study revealed the expression of STC2 in NSPCs derived from the SVZ of the C57BL/6N mouse. In cultured SVZ-derived NSPCs, STC2 treatment significantly increased the number of Tuj1 and DCX-positive cells. Furthermore, STC2 injection into the lateral ventricle promoted the neuronal differentiation of NSPCs and migration to the olfactory bulb. Conversely, the STC2 knockdown produced the opposite effect. Further investigation showed that STC2 treatment enhanced AKT phosphorylation in cultured NSPCs, whereas STC2 inhibition hindered AKT activation. Notably, the neuronal differentiation induced by STC2 was blocked by the AKT inhibitor GSK690693, whereas the AKT activator SC79 reversed the impact of STC2 knockdown on neuronal differentiation. Our findings indicate that enhancing STC2 expression in SVZ-derived NSPCs facilitates neuronal differentiation, with AKT regulation potentially serving as a key intracellular target of STC2 signaling.

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