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- Yuyong Chen, Lei He, Mao Pang, Zekai Ke, Xiaozuo Zheng, Feng Feng, Bu Yang, Nanxiang Wang, Bin Liu, Tao Wu, and Tao Shu.
- Department of Spine Surgery, The 3rd Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, China; Guangdong Provincial Center for Quality Control of Minimally Invasive Spine Surgery, Guangzhou, Guangdong 510630, China; Guangdong Provincial Center for Engineering and Technology Research of Minimally Invasive Spine Surgery, Guangzhou, Guangdong 510630, China.
- Neuroscience. 2020 Oct 15; 446: 69-79.
AbstractMelatonin is crucial for protecting neural stem cells (NSCs) from reactive oxygen species (ROS). However, the mechanism underlying these processes is unclear. In this study, we first investigated the significantly upregulated lncRNA MEG3 biomarker in the H2O2-induced NSCs and control groups. Melatonin inhibited the expression of MEG3 by methylation. MEG3 overexpression reversed the positive effects of melatonin on NSCs against H2O2. Furthermore, MEG3 reduced the expression levels of its targeted miRNA-27a-3p, which could be considered a neuroprotective effect. In addition, the elevated miRNA-27a-3p decreased JNK phosphorylation by targeting MAP2K4. Overexpression of MAP2K4 suppressed the neuroprotective effects of miRNA-27a-3p. Therefore, melatonin appeared to protect NSCs from H2O2-induced ROS by modification of the MEG3/miRNA-27a-3p/MAP2K4 axis.Copyright © 2020 IBRO. Published by Elsevier Ltd. All rights reserved.
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