Inhibition of miR-200b/miR-429 Contributes to Neuropathic Pain development Through Targeting Zinc finger E box binding protein-1.

Inhibition of miR-200b/miR-429 Contributes to Neuropathic Pain development Through Targeting Zinc finger E box binding protein-1.

J Cell Physiol. 2017 Nov 18;:

Authors: Yan XT, Zhao Y, Cheng XL, He XH, Wang Y, Zheng WZ, Chen H, Wang YL

Abstract
Many studies have reported that microRNAs participate in neuropathic pain development. Previously, miR-200b and miR-429 are reported to be involved in various diseases. In our current study, we focused on their roles in neuropathic pain and we found that miR-200b and miR-429 were significantly decreased in chronic constriction injury (CCI) rat spinal cords and isolated microglials. miR-200b and miR-429 overexpression were able to relieve neuropathic pain through modulating PWT and PWL in CCI rats. Meanwhile, we observed that both miR-200b and miR-429 upregulation could repress neuroinflammation via inhibiting inflammatory cytokines such as IL-6, IL-1β and TNF-α in CCI rats. By carry out bioinformatics technology, Zinc finger E box binding protein-1 (ZEB1) was predicted as target of miR-200b and miR-429 and dual-luciferase reporter assays confirmed the correlation between them. ZEB1 has been reported to regulate a lot of diseases. Here, we found that ZEB1 was greatly increased in CCI rats and miR-200b and miR-429 overexpression markedly suppressed ZEB1 mRNA expression in rat microglial cells. In addition, knockdown of ZEB1 can reduce neuropathic pain development and co-transfection of LV-anti-miR-200b/miR-429 reversed this phenomenon in vivo. Taken these together, our results suggested that miR-200b/miR-429 can serve as an important regulator of neuropathic pain development by targeting ZEB1. This article is protected by copyright. All rights reserved.

PMID: 29150958 [PubMed - as supplied by publisher]

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