z-logo
Premium
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.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom