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miR‐124‐3p attenuates neuropathic pain induced by chronic sciatic nerve injury in rats via targeting EZH2
Author(s) -
Zhang Yang,
Liu HaiLin,
An LiJun,
Li Lin,
Wei Meng,
Ge DongJian,
Su Zhen
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27861
Subject(s) - neuropathic pain , medicine , sciatic nerve injury , sciatic nerve , nerve injury , ezh2 , chronic pain , pharmacology , anesthesia , chemistry , physical therapy , epigenetics , biochemistry , gene
Emerging evidence has suggested that microRNAs play a critical role in neuropathic pain development. However, the biological role of miRNAs in regulating neuropathic pain remains barely known. In our present study, we found that miR‐124‐3p was significantly downregulated in rats after chronic sciatic nerve injury (CCI). In addition, it was showed that overexpression of miR‐124‐3p obviously repressed mechanical allodynia and heat hyperalgesia. Meanwhile, it has been reported that neuroinflammation can contribute a lot to neuropathic pain progression. Here, we found that inflammatory cytokine (IL‐6, IL‐1β, and TNF‐⍺) protein expression in rats after CCI greatly increased and miR‐124‐3p mimics depressed inflammation cytokine levels. Consistently, miR‐124‐3p alleviated inflammation production in lipopolysaccharide‐incubated spinal microglial cells. Bioinformatics analysis revealed that EZH2 acted as a direct target of miR‐124‐3p, which participated in the miR‐124‐3p‐modulated effects on neuropathic pain development and neuroinflammation. We observed that miR‐124‐3p was able to promote neuroinflammation and neuropathic pain through targeting EZH2. The direct correlation between them was validated in our current study using dual‐luciferase reporter assays. Subsequently, it was manifested that EZH2 abrogated the inhibitory role of miR‐124‐3p on neuropathic pain progression in CCI rats. Taken these together, our findings highlighted a novel contribution of miR‐124‐3p to neuropathic pain and indicated the possibilities for developing novel therapeutic options for neuropathic pain.