PMID- 24612023
OWN - NLM
STAT- MEDLINE
DCOM- 20150106
LR  - 20140519
IS  - 1460-9568 (Electronic)
IS  - 0953-816X (Linking)
VI  - 39
IP  - 10
DP  - 2014 May
TI  - Intrathecal miR-183 delivery suppresses mechanical allodynia in mononeuropathic 
      rats.
PG  - 1682-9
LID - 10.1111/ejn.12522 [doi]
AB  - Members of the miR-183 family are unique in that they are highly abundant in 
      sensory organs. In a recent study, significant downregulation was observed for 
      miR-96 and miR-183 in the L5 dorsal root ganglion (DRG) 2 weeks after spinal 
      nerve ligation (SNL). In this study, we focused on miR-183, which is the most 
      regulated member of the miR-183 family, to look at the specific role on 
      neuropathic pain. Persistent mechanical allodynia was induced with the L5 SNL 
      model in 8-week-old male Sprague-Dawley rats. Paw withdrawal thresholds in 
      response to mechanical stimuli were assessed with Von Frey filaments. Expression 
      of miR-183 in the L5 DRG was assessed with quantitative real-time polymerase 
      chain reaction (qPCR) analysis. Lentivirions expressing miR-183 were injected 
      intrathecally into SNL rats. Changes in mechanical allodynia were assessed with 
      Von Frey filaments. In addition, changes in the predicted target genes of miR-183 
      were assessed with qPCR. L5 SNL produced marked mechanical allodynia in the 
      ipsilateral hindpaws of adult rats, beginning at postoperative day 1 and 
      continuing to day 14. L5 SNL caused significant downregulation of miR-183 in 
      adult DRG cells. Intrathecal administration of lentivirions expressing miR-183 
      downregulated SNL-induced increases in the expression of Nav1.3 and brain-derived 
      neurotrophic factor (BDNF), which correlated with the significant attenuation of 
      SNL-induced mechanical allodynia. Our results show that SNL-induced mechanical 
      allodynia is significantly correlated with the decreased expression of miR-183 in 
      DRG cells. Replacement of miR-183 downregulates SNL-induced increases in Nav1.3 
      and BDNF expression, and attenuates SNL-induced mechanical allodynia.
CI  - (c) 2014 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.
FAU - Lin, Chung-Ren
AU  - Lin CR
AD  - Department of Anesthesiology, Kaohsiung Chang Gung Memorial Hospital and Chang 
      Gung University College of Medicine, No. 123 Dapi Rd, Kaohsiung, 833, Taiwan; 
      Department of Anesthesiology, National Taiwan University College of Medicine, 
      Taipei, Taiwan.
FAU - Chen, Kuan-Hung
AU  - Chen KH
FAU - Yang, Chien-Hui
AU  - Yang CH
FAU - Huang, Hui-Wen
AU  - Huang HW
FAU - Sheen-Chen, Shyr-Ming
AU  - Sheen-Chen SM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140311
PL  - France
TA  - Eur J Neurosci
JT  - The European journal of neuroscience
JID - 8918110
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (MIRN183 microRNA, rat)
RN  - 0 (MicroRNAs)
RN  - 0 (NAV1.3 Voltage-Gated Sodium Channel)
RN  - 0 (Scn3a protein, rat)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Disease Models, Animal
MH  - Down-Regulation
MH  - Ganglia, Spinal/*physiopathology
MH  - Gene Transfer Techniques
MH  - Genetic Vectors
MH  - Hyperalgesia/*physiopathology
MH  - Lentivirus/genetics
MH  - Male
MH  - MicroRNAs/genetics/*metabolism
MH  - NAV1.3 Voltage-Gated Sodium Channel/metabolism
MH  - Neuralgia/physiopathology
MH  - Pain Threshold/physiology
MH  - Physical Stimulation
MH  - Rats, Sprague-Dawley
MH  - Real-Time Polymerase Chain Reaction
MH  - Spinal Nerves/injuries
MH  - Touch
OTO - NOTNLM
OT  - intrathecal delivery
OT  - lentivirions
OT  - neuropathic pain
OT  - spinal nerve ligation
EDAT- 2014/03/13 06:00
MHDA- 2015/01/07 06:00
CRDT- 2014/03/12 06:00
PHST- 2013/09/26 00:00 [received]
PHST- 2014/01/08 00:00 [revised]
PHST- 2014/01/27 00:00 [accepted]
PHST- 2014/03/12 06:00 [entrez]
PHST- 2014/03/13 06:00 [pubmed]
PHST- 2015/01/07 06:00 [medline]
AID - 10.1111/ejn.12522 [doi]
PST - ppublish
SO  - Eur J Neurosci. 2014 May;39(10):1682-9. doi: 10.1111/ejn.12522. Epub 2014 Mar 11.