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超声刺激通过激活雷帕霉素哺乳动物靶蛋白增加损伤背根神经节神经元的神经突再生。

Ultrasound Stimulation Increases Neurite Regeneration in Injured Dorsal Root Ganglion Neurons through Mammalian Target of Rapamycin Activation.

作者信息

Han Sungmin, Park Jinyoung, Choi Won Seok, Youn Inchan

机构信息

Biomedical Research Institute, Korea Institute of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Korea.

Molecular Recognition Research Center, Korea Institute of Science and Technology, Hwarangno 14-gil 5, Seongbuk-gu, Seoul 02792, Korea.

出版信息

Brain Sci. 2020 Jun 30;10(7):409. doi: 10.3390/brainsci10070409.

Abstract

Ultrasound stimulation (US) is reported to be a safe and useful technology for improving injured nerve regeneration. However, the intracellular mechanisms underlying its stimulatory effects are only partially understood. Mammalian target of rapamycin (mTOR) signaling is involved in neuronal survival and axonal outgrowth. In this study, we investigated the effect of US on regeneration of injured dorsal root ganglion (DRG) neurons and activation of the mTOR pathway. We showed that US significantly increased neurite regeneration and enhanced mTOR activation. Moreover, the expression of growth-associated protein-43 (GAP-43), a crucial factor for axonal outgrowth and regeneration in neurons, was significantly increased by US. These data suggest that US-induced neurite regeneration is mediated by upregulation of mTOR activity, which promotes the regeneration of injured DRG neurons.

摘要

据报道,超声刺激(US)是一种用于促进受损神经再生的安全且有用且安全有效的技术。然而,其刺激作用背后的细胞内机制仅得到部分理解。雷帕霉素哺乳动物靶点(mTOR)信号传导参与神经元存活和轴突生长。在本研究中,我们调查了超声刺激对受损背根神经节(DRG)神经元再生以及mTOR通路激活的影响。我们发现,超声刺激显著增加了神经突再生并增强了mTOR激活。此外,超声刺激使生长相关蛋白43(GAP - 43)的表达显著增加,GAP - 43是神经元轴突生长和再生的关键因子。这些数据表明超声刺激诱导的神经突再生是由mTOR活性上调介导的,mTOR活性上调促进了受损DRG神经元的再生。

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