Laboratory Animal Research Center of Shanxi Medical University, Shanxi Key Laboratory of Animal and Animal Model of Human Diseases, Taiyuan 030001, China.
Queen Mary School, Nanchang University, Nanchang 330000, China.
Exp Biol Med (Maywood). 2021 Jun;246(11):1274-1286. doi: 10.1177/1535370221997071. Epub 2021 Mar 9.
This study aims to examine whether miR-31 promotes endogenous NSC proliferation and be used for spinal cord injury management. In the present study, the morpholino knockdown of miR-31 induced abnormal neuronal apoptosis in zebrafish, resulting in impaired development of the tail. miR-31 agomir transfection in NSCs increased Nestin expression and decreased ChAT and GFAP expression levels. miR-31 induced the proliferation of mouse NSCs by upregulating the Notch signaling pathway, and more NSCs entered G1; Notch was inhibited by miR-31 inactivation. Injection of a miR-31 agomir into mouse models of spinal cord injury could effectively restore motor functions after spinal cord injury, which was achieved by promoting the proliferation of endogenous NSCs. After the injection of a miR-31 agomir in spinal cord injury mice, the expression of Nestin and GFAP increased, while GFAP expression decreased. In conclusion, the zebrafish experiments prove that a lack of miR-31 will block nervous system development. In spinal cord injury mouse models, miR-31 overexpression might promote spinal cord injury repair.
本研究旨在探讨 miR-31 是否能促进内源性 NSC 增殖，并用于脊髓损伤的治疗。在本研究中，miR-31 的形态发生抑制导致斑马鱼神经元凋亡异常，从而损害尾巴的发育。miR-31 激动剂转染 NSCs 增加了 Nestin 的表达，降低了 ChAT 和 GFAP 的表达水平。miR-31 通过上调 Notch 信号通路诱导小鼠 NSCs 的增殖，使更多的 NSCs 进入 G1 期；miR-31 的失活抑制了 Notch。向脊髓损伤小鼠模型中注射 miR-31 激动剂可通过促进内源性 NSCs 的增殖有效恢复脊髓损伤后的运动功能。在脊髓损伤小鼠中注射 miR-31 激动剂后，Nestin 和 GFAP 的表达增加，而 GFAP 的表达减少。总之，斑马鱼实验证明 miR-31 的缺失会阻断神经系统的发育。在脊髓损伤小鼠模型中，miR-31 的过表达可能促进脊髓损伤的修复。
