褪黑素通过lncRNA MEG3/miRNA-27a-3p/MAP2K4轴促进HO诱导的神经干细胞的神经保护作用。
Melatonin Promotes Neuroprotection of HO-induced Neural Stem Cells via lncRNA MEG3/miRNA-27a-3p/MAP2K4 axis.
作者信息
Chen Yuyong, He Lei, Pang Mao, Ke Zekai, Zheng Xiaozuo, Feng Feng, Yang Bu, Wang Nanxiang, Liu Bin, Wu Tao, Shu Tao
机构信息
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.
Department of Orthopaedic Surgery, Shenzhen University General Hospital, Shenzhen, Guangdong 518055, China.
出版信息
Neuroscience. 2020 Oct 15;446:69-79. doi: 10.1016/j.neuroscience.2020.06.026. Epub 2020 Jun 26.
Melatonin 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 HO-induced NSCs and control groups. Melatonin inhibited the expression of MEG3 by methylation. MEG3 overexpression reversed the positive effects of melatonin on NSCs against HO. 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 HO-induced ROS by modification of the MEG3/miRNA-27a-3p/MAP2K4 axis.
褪黑素对于保护神经干细胞（NSCs）免受活性氧（ROS）的损伤至关重要。然而，这些过程背后的机制尚不清楚。在本研究中，我们首先调查了HO诱导的神经干细胞组和对照组中显著上调的lncRNA MEG3生物标志物。褪黑素通过甲基化抑制MEG3的表达。MEG3过表达逆转了褪黑素对HO处理的神经干细胞的积极作用。此外，MEG3降低了其靶向的miRNA-27a-3p的表达水平，这可被视为一种神经保护作用。另外，升高的miRNA-27a-3p通过靶向MAP2K4降低JNK磷酸化。MAP2K4过表达抑制了miRNA-27a-3p的神经保护作用。因此，褪黑素似乎通过修饰MEG3/miRNA-27a-3p/MAP2K4轴来保护神经干细胞免受HO诱导的ROS损伤。
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