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Regulation of μ‐opioid type 1 receptors by micro RNA 134 in dorsal root ganglion neurons following peripheral inflammation
Author(s) -
Ni J.,
Gao Y.,
Gong S.,
Guo S.,
Hisamitsu T.,
Jiang X.
Publication year - 2013
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1002/j.1532-2149.2012.00197.x
Subject(s) - dorsal root ganglion , receptor , opioid , in situ hybridization , inflammation , gene expression , microbiology and biotechnology , messenger rna , chemistry , pathophysiology , pharmacology , biology , medicine , gene , spinal cord , neuroscience , biochemistry
Background MOR 1 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. Micro RNA s (mi R ) 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 mi R ‐134 was found in 3′‐untranslated region of MOR 1. Given the important roles of MOR 1 in pain modulation, the purpose of this study is to investigate whether mi R ‐134 can regulate the MOR 1 following allodynia. Methods Using F reund's adjuvant ( CFA )‐induced chronic inflammatory pain model, we investigated the expression profiles of mi R ‐134 and MOR 1 in rat dorsal root ganglia ( DRG ) using quantitative real‐time polymerase chain reaction, in situ hybridization and immunohistochemistry, respectively. The relationship of mi R ‐134 and MOR 1 expressions was analysed by linear regression. Luciferase assay was used to examine whether MOR 1 was the target of mi R ‐134. Results Our results showed that mi R ‐134 expression level was inversely related to MOR 1 expression. Down‐regulation of mi R ‐134 and up‐regulation of MOR 1 in the same tissues after inflammatory pain were observed. Functional experiments showed that MOR 1 expression in SH ‐ SY5Y cells was up‐regulated after inhibition of mi R ‐134, indicating that MOR 1 was a target of mi R ‐134. Conclusions Our present data suggested a model that mi R ‐134 participated in CFA ‐induced inflammatory pain by balancing the expression of MOR 1 in DRGs , which implied that mi R ‐134 may be a potential therapeutic target for the treatment of neuropathic pain including inflammation.