Open AccessmiR-31 promotes neural stem cell proliferation and restores motor function after spinal cord injury
Author(s) -
Xiao Li,
Yuantao Gao,
Feng Tian,
Ruochen Du,
Yitong Yuan,
Pengfei Li,
Fang Liu,
Chunfang Wang
Publication year - 2021
Publication title -
experimental biology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 146
eISSN - 1535-3702
pISSN - 1535-3699
DOI - 10.1177/1535370221997071
Subject(s) - spinal cord injury , spinal cord , neural stem cell , gene knockdown , zebrafish , nestin , endogeny , microbiology and biotechnology , biology , neuroscience , notch signaling pathway , medicine , apoptosis , stem cell , signal transduction , gene , biochemistry
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.