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, 17 (3), 313-23

Regulation of μ-Opioid Type 1 Receptors by microRNA134 in Dorsal Root Ganglion Neurons Following Peripheral Inflammation

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Regulation of μ-Opioid Type 1 Receptors by microRNA134 in Dorsal Root Ganglion Neurons Following Peripheral Inflammation

J Ni et al. Eur J Pain.

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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