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Rab11 promotes single Mauthner cell axon regeneration in vivo through axon guidance molecule Ntng2b.
Experimental Neurology ( IF 4.6 ) Pub Date : 2024-02-05 , DOI: 10.1016/j.expneurol.2024.114715
Huaitong Yao 1 , Yueru Shen 1 , Zheng Song 1 , Along Han 1 , Xinghan Chen 1 , Yawen Zhang 1 , Bing Hu 2
Affiliation  

Effective axon regeneration within the central nervous system (CNS) is pivotal for achieving functional recovery following spinal cord injury (SCI). Numerous extrinsic and intrinsic factors exert influences on the axon regeneration. While prior studies have demonstrated crucial involvement of specific members the Rab protein family in axon regeneration in the peripheral nervous system (PNS), the precise function of Rab11 in CNS axon regeneration remains elusive. Thus, our study aimed to elucidate the impact of Rab11 on the axon regeneration of Mauthner cells (M-cells) in zebrafish larvae. Our findings demonstrated that overexpression of Rab11bb single-cell electroporation significantly promoted axon regeneration in individual M-cells. Conversely, knockdown of Rab11bb inhibited the axon regeneration of M-cells. RNA-seq analysis revealed an upregulation of following Rab11bb overexpression. As we hypothesized, overexpression of Ntng2b markedly enhanced axon regeneration, while Ntng2b knockdown in the context of Rab11bb pro-regeneration substantially hindered axon regrowth. In conclusion, our study demonstrated that Rab11 promotes axon regeneration of single M-cell in the CNS through the Rab11/axon guidance/Ntng2b pathway.

中文翻译:


Rab11 通过轴突引导分子 Ntng2b 促进体内单 Mauthner 细胞轴突再生。



中枢神经系统 (CNS) 内有效的轴突再生对于脊髓损伤 (SCI) 后实现功能恢复至关重要。许多外在和内在因素对轴突再生产生影响。虽然之前的研究已经证明 Rab 蛋白家族的特定成员在周围神经系统 (PNS) 轴突再生中发挥着重要作用,但 Rab11 在 CNS 轴突再生中的确切功能仍然难以捉摸。因此,我们的研究旨在阐明 Rab11 对斑马鱼幼虫 Mauthner 细胞(M 细胞)轴突再生的影响。我们的研究结果表明,Rab11bb 单细胞电穿孔的过度表达显着促进单个 M 细胞的轴突再生。相反,敲低 Rab11bb 会抑制 M 细胞的轴突再生。 RNA-seq 分析揭示了 Rab11bb 过度表达后的上调。正如我们假设的,Ntng2b 的过度表达显着增强了轴突再生,而 Rab11bb 促再生背景下的 Ntng2b 敲低则显着阻碍了轴突再生。总之,我们的研究表明 Rab11 通过 Rab11/轴突引导/Ntng2b 途径促进中枢神经系统中单个 M 细胞的轴突再生。
更新日期:2024-02-05
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