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

, : Regulation of μ-opioid type 1 receptors by microRNA134 in dorsal root ganglion neurons following peripheral inflammation. European Journal of Pain 17(3): 313-323

MOR1 is the main transcript of ?-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 MORGiven 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. 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. 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. 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.


PMID: 22865422

DOI: 10.1002/j.1532-2149.2012.00197.x

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