The role of miR-190a-5p contributes to diabetic neuropathic pain via targeting SLC17A6
Authors Yang D, Yang Q, Wei X, Liu Y, Ma D, Li J, Wan Y, Luo Y
Received 2 February 2017
Accepted for publication 20 April 2017
Published 4 October 2017 Volume 2017:10 Pages 2395—2403
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Amy Norman
Peer reviewer comments 3
Editor who approved publication: Dr Katherine Hanlon
Di Yang*, Qinyan Yang*, Xinchuan Wei, Yang Liu, Ding Ma, Jiaceng Li, Yongling Wan, Yao Luo
Department of Anesthesiology, Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China
*These authors contributed equally to this work
Introduction: MicroRNAs play a key role in neuropathic pain. In a previous study, miR-190a-5p was significantly downregulated in diabetic neuropathic pain (DNP). However, the role and pathological mechanism of miR-190a-5p in DNP still remain unclear.
Materials and methods: DNP model was established. The paw withdrawal thresholds were measured to assess the mechanical nociceptive response. Dual-luciferase reporter assay was used to confirm the target gene of microRNA. The expressions of microRNA, gene, and protein were detected by the quantitative real-time polymerase chain reaction or Western blot. The levels of IL-1β and IL-6 were detected with the enzyme-linked immuno sorbent assay.
Results: Compared with the control sample, the expression of miR-190a-5p was decreased and SLC17A6 was increased in the spinal tissue from those developing DNP. The bioinformatics and luciferase reporter assay demonstrated that SLC17A6 is a direct target of miR-190a-5p. Up-regulation of miR-190a-5p and inhibition of SLC17A6 could significantly weaken the painful behavior and reduce IL-1β and IL-6 level in DNP.
Conclusion: miR-190a-5p is involved in DNP via targeting SLC17A6, and miR-190a-5p and SLC17A6 may be the therapeutic targets of this disease.
Keywords: miR-190a-5p, DNP, spinal tissue, painful behavior, IL-1β and IL-6, SLC17A66