title: Regulation of μ-opioid type 1 receptors by microRNA134 in dorsal root ganglion neurons following peripheral inflammation.
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.
authors.affiliation: Key Laboratory of Pain Basic Research & Clinical Therapy, Department of Neurobiology, Medical College of Soochow University, Suzhou, China.
authors.forename: J
authors.initials: J
authors.lastname: Ni
authors.forename: Y
authors.initials: Y
authors.lastname: Gao
authors.forename: S
authors.initials: S
authors.lastname: Gong
authors.forename: S
authors.initials: S
authors.lastname: Guo
authors.forename: T
authors.initials: T
authors.lastname: Hisamitsu
authors.forename: X
authors.initials: X
authors.lastname: Jiang
mesh_terms: D020413:3' Untranslated Regions / Q000235:genetics; D000818:Animals; D015153:Blotting, Western; D002460:Cell Line; D005455:Fluorescent Antibody Technique; D005727:Ganglia, Spinal / Q000378:metabolism* / Q000503:physiopathology; D006358:Hot Temperature; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007249:Inflammation / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D035683:MicroRNAs / Q000502:physiology*; D009474:Neurons / Q000378:metabolism* / Q000502:physiology; D010146:Pain / Q000235:genetics / Q000503:physiopathology; D010147:Pain Measurement; D010523:Peripheral Nervous System Diseases / Q000378:metabolism* / Q000503:physiopathology; D010812:Physical Stimulation; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D060888:Real-Time Polymerase Chain Reaction; D017450:Receptors, Opioid, mu / Q000096:biosynthesis*
chemical_list: D020413:3' Untranslated Regions; C581995:MIRN134 microRNA, rat; D035683:MicroRNAs; C485765:Oprm1 protein, rat; D012333:RNA, Messenger; D017450:Receptors, Opioid, mu