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Regulation of μ-opioid type 1 receptors by microRNA134 in dorsal root ganglion neurons following peripheral inflammation

Authors


  • Funding sources

    This study is supported by the Natural Science Funding of Jiangsu Province Grant (BK2009118), the Doctoral Program of Higher Education of China (20093201110018), the Specialized Research Fund for the Doctoral Program of Higher Education (CX09B_032Z), and a project funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions.

  • Conflicts of interest

    No potential conflicts of interest were disclosed.

Correspondence

Xinghong Jiang

E-mail: jiangxinghong@suda.edu.cn

Abstract

Background

MOR1 is the main transcript of μ-opioid receptor (MOR) gene, which represents a mandatory molecule for the analgesic effects of opioids and plays an important role in the pathology of inflammatory pain. MicroRNAs (miR) are non-coding molecules that primarily modulate gene expression at the post-transcriptional level in various pathophysiological conditions. Based on in silico analysis, an exact match to the seed sequence of miR-134 was found in 3′-untranslated region of MOR1. Given the important roles of MOR1 in pain modulation, the purpose of this study is to investigate whether miR-134 can regulate the MOR1 following allodynia.

Methods

Using Freund's adjuvant (CFA)-induced chronic inflammatory pain model, we investigated the expression profiles of miR-134 and MOR1 in rat dorsal root ganglia (DRG) using quantitative real-time polymerase chain reaction, in situ hybridization and immunohistochemistry, respectively. The relationship of miR-134 and MOR1 expressions was analysed by linear regression. Luciferase assay was used to examine whether MOR1 was the target of miR-134.

Results

Our results showed that miR-134 expression level was inversely related to MOR1 expression. Down-regulation of miR-134 and up-regulation of MOR1 in the same tissues after inflammatory pain were observed. Functional experiments showed that MOR1 expression in SH-SY5Y cells was up-regulated after inhibition of miR-134, indicating that MOR1 was a target of miR-134.

Conclusions

Our present data suggested a model that miR-134 participated in CFA-induced inflammatory pain by balancing the expression of MOR1 in DRGs, which implied that miR-134 may be a potential therapeutic target for the treatment of neuropathic pain including inflammation.

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