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NeuroD1 overexpression in spinal neurons accelerates axonal regeneration after sciatic nerve injury.
Experimental Neurology ( IF 4.6 ) Pub Date : 2020-01-25 , DOI: 10.1016/j.expneurol.2020.113215
Muhua Lai 1 , Mengjie Pan 2 , Longjiao Ge 3 , Jingmin Liu 1 , Junyao Deng 1 , Xianghai Wang 1 , Lixia Li 1 , Jinkun Wen 1 , Dandan Tan 1 , Haowen Zhang 1 , Xiaofang Hu 1 , Lanya Fu 1 , Yizhou Xu 1 , Zhenlin Li 1 , Xiaozhong Qiu 4 , Gong Chen 5 , Jiasong Guo 6
Affiliation  

Neurogenic differentiation 1 (NeuroD1) is mainlyexpressed in developing neurons where it plays critical roles in neuronal maturation and neurite elongation. The potential role and mechanism of NeuroD1 in adult axonal regeneration is not clear. The present study used synapsin (SYN) Cre and AAV9-Flex vectors to conditionally overexpress NeuroD1 in adult spinal neurons and found that NeuroD1 overexpression significantly accelerated axonal regeneration and functional recovery after sciatic nerve injury. Further in vitro and in vivo experiments suggested that the mechanism of NeuroD1 promotion on axonal regeneration was related to its regulation of the expression of neurotrophin BDNF and its receptor TrkB as well as a microtubule severing protein spastin.

中文翻译:

脊髓神经元中的 NeuroD1 过表达加速了坐骨神经损伤后的轴突再生。

神经源性分化 1 (NeuroD1) 主要在发育中的神经元中表达,在神经元成熟和神经突伸长中起关键作用。NeuroD1 在成人轴突再生中的潜在作用和机制尚不清楚。本研究使用突触蛋白 (SYN) Cre 和 AAV9-Flex 载体在成人脊髓神经元中有条件地过表达 NeuroD1,发现 NeuroD1 过表达显着加速了坐骨神经损伤后的轴突再生和功能恢复。进一步的体外和体内实验表明,NeuroD1促进轴突再生的机制与其调节神经营养因子BDNF及其受体TrkB以及微管切断蛋白spastin的表达有关。
更新日期:2020-01-26
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