Melatonin benefits to the growth of human annulus fibrosus cells through inhibiting miR-106a-5p/ATG7 signaling pathway
Received 7 November 2018
Accepted for publication 18 February 2019
Published 28 March 2019 Volume 2019:14 Pages 621—630
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 3
Editor who approved publication: Dr Zhi-Ying Wu
Bao Hai,1 Yunlong Ma,2 Xiaoyu Pan,1 Lei Yong,1 Chen Liang,1 Guanping He,1 Chenlong Yang,1 Bin Zhu,2 Xiaoguang Liu1
1Department of Orthopedics, Peking University Third Hospital, Beijing 100191, People’s Republic of China; 2The Center for Pain Medicine, Peking University Third Hospital, Beijing 100191, People’s Republic of China
Background: Disc degeneration (DD) is one of the common diseases worldwide, which deeply influences normal life and leads to excruciating pain. However, an effective treatment for DD is still not identified.
Method: The present study systemically examined the effect of melatonin on annulus fibrosus (AF) cells of patients with DD.
Results: Melatonin had the effect of promoting proliferation, inducing autophagy, and suppressing apoptosis on AF cells of patients with DD. Moreover, melatonin contributed to the translation and transcription of autophagy-related protein ATG7 and inhibited the function of miR-106a-5p in AF cells. In addition, the results suggested that miR-106a-5p mediated the expression of ATG7 by directly binding to its 3'UTR in AF cells.
Conclusion: This research not only gained a deep insight of melatonin mode of action, but also indicated its potential target signaling pathway in AF cells.
Keywords: disc degeneration, melatonin, ATG7, miR-106a-5p
This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.Download Article [PDF] View Full Text [HTML][Machine readable]