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Effects of miR-26a-5p on neuropathic pain development by targeting MAPK6 in in CCI rat models

Yang Zhang1, Zhen Su1, Hai-Lin Liu1

  • 1Department of Anesthesiology, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu, 223300, PR China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|August 18, 2018
PubMed

Insights

MicroRNA-26a-5p (miR-26a-5p) levels decrease in neuropathic pain. Restoring miR-26a-5p alleviates pain and neuroinflammation by targeting MAPK6, suggesting miR-26a-5p as a potential therapeutic target.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pain Research

Background:

  • MicroRNAs (miRNAs) are key regulators in neuropathic pain.
  • Neuroinflammation significantly contributes to neuropathic pain development.
  • The specific role of miR-26a-5p in neuropathic pain and neuroinflammation remains largely unexplored.

Purpose of the Study:

  • To investigate the function of miR-26a-5p in neuropathic pain.
  • To elucidate the underlying molecular mechanisms involving miR-26a-5p in neuroinflammation and pain progression.

Main Methods:

  • Established a rat model of neuropathic pain using chronic sciatic nerve injury (CCI).
  • Quantified miR-26a-5p expression in spinal cord tissues.
  • Overexpressed miR-26a-5p and assessed its effects on pain behavior and neuroinflammation.
  • Identified and validated MAPK6 as a direct downstream target of miR-26a-5p using dual-luciferase reporter assays.
  • Examined the correlation between MAPK6 and miR-26a-5p expression in CCI rats.
  • Investigated the effect of MAPK6 upregulation on miR-26a-5p's therapeutic actions.

Main Results:

  • miR-26a-5p expression was significantly downregulated in the spinal cords of CCI rats compared to controls.
  • Overexpression of miR-26a-5p markedly reduced neuropathic pain and neuroinflammation in CCI rats.
  • MAPK6 was confirmed as a direct target of miR-26a-5p, with miR-26a-5p overexpression reducing MAPK6 levels both in vitro and in vivo.
  • MAPK6 expression showed an inverse correlation with miR-26a-5p levels in CCI rats.
  • Upregulation of MAPK6 reversed the beneficial effects of miR-26a-5p on neuroinflammation and neuropathic pain.

Conclusions:

  • miR-26a-5p acts as a negative regulator in the development of neuropathic pain.
  • The mechanism involves the direct targeting of MAPK6 by miR-26a-5p.
  • miR-26a-5p presents a promising therapeutic target for managing neuropathic pain and associated neuroinflammation.
Keywords:
MAPK6NeuroinflammationNeuropathic painmiR26a-5p

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