Regulation of μ‐opioid type 1 receptors by microRNA134 in dorsal root ganglion neurons following peripheral inflammation. (3rd August 2012)

• Record Type: Journal Article
• Authors: Ni, J.; Gao, Y.; Gong, S.; Guo, S.; Hisamitsu, T.; Jiang, X.
• Is Part Of: European journal of pain. Volume 17:Number 3(2013)
• Page Start: 313
• Page End: 323
• Publication Date: 2012-08-03
• Subjects: Pain -- Periodicals; Pain -- Treatment -- Periodicals; Pain -- Physiological aspects -- Periodicals; 616.0472
• DOI: 10.1002/j.1532-2149.2012.00197.x
• Languages: English
• ISSNs: 1090-3801

Abstract

<abstract abstract-type="main"> <title>Abstract</title> <sec id="ejp197-sec-0001" sec-type="section"> <title>Background</title> <p>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 <italic>in silico</italic> 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.</p> </sec> <sec id="ejp197-sec-0002" sec-type="section"> <title>Methods</title> <p>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, <italic>in situ</italic> 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.</p> </sec> <sec id="ejp197-sec-0003" sec-type="section"> <title>Results</title> <p>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.</p> </sec> <sec id="ejp197-sec-0004" sec-type="section"> <title>Conclusions</title> <p>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.</p> </sec> </abstract>