PMID- 28629826
OWN - NLM
STAT- MEDLINE
DCOM- 20170918
LR  - 20170918
IS  - 1879-0038 (Electronic)
IS  - 0378-1119 (Linking)
VI  - 627
DP  - 2017 Sep 5
TI  - Silencing of FKBP51 alleviates the mechanical pain threshold, inhibits DRG 
      inflammatory factors and pain mediators through the NF-kappaB signaling pathway.
PG  - 169-175
LID - S0378-1119(17)30479-1 [pii]
LID - 10.1016/j.gene.2017.06.029 [doi]
AB  - Neuropathic pain is chronic pain caused by lesions or diseases of the 
      somatosensory system, currently available analgesics provide only temporal 
      relief. The precise role of FK506 binding protein 51 (FKBP51) in neuropathic pain 
      induced by chronic constriction injury (CCI) is not clear. The purpose of the 
      present study was to investigate the effects and possible mechanisms of FKBP51 in 
      neuropathic pain in the rat model of CCI. Our results showed that FKBP51 was 
      obviously upregulated in a time-dependent manner in the dorsal root ganglion 
      (DRG) of CCI rats. Additionally, silencing of FKBP51 remarkably attenuated 
      mechanical allodynia and thermal hyperalgesia as reflected by paw withdrawal 
      threshold (PWT) and paw withdrawal latency (PWL) in CCI rats. Moreover, knockdown 
      of FKBP51 reduced the production of pro-inflammatory cytokines (TNF-alpha, IL-1beta and 
      IL-6), nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) 
      expression in the DRG of CCI rats. Furthermore, we revealed that inhibition of 
      FKBP51 greatly suppressed the activation of the NF-kappaB (NF-kappaB) signaling in 
      the DRG of CCI rats. Interestingly, similar to the FKBP51 siRNA (si-FKBP51), 
      ammonium pyrrolidinedithiocarbamate (PDTC, an inhibitor of NF-kappaB) also alleviated 
      neuropathic pain and neuro-inflammation, indicating that knockdown of FKBP51 
      alleviated neuropathic pain development of CCI rats by inhibiting the activation 
      of NF-kappaB signaling pathway. Taken together, our findings indicate that FKBP51 may 
      serve as a novel therapeutic target for neuropathic pain.
CI  - Copyright (c) 2017. Published by Elsevier B.V.
FAU - Yu, Hong-Mei
AU  - Yu HM
AD  - Department of Anesthesia, Cangzhou Central Hospital, Cangzhou 061000, PR China. 
      Electronic address: hongmeiyuhmy@163.com.
FAU - Wang, Qi
AU  - Wang Q
AD  - Department of Anesthesia, Cangzhou Central Hospital, Cangzhou 061000, PR China.
FAU - Sun, Wen-Bo
AU  - Sun WB
AD  - Department of Anesthesia, Cangzhou Central Hospital, Cangzhou 061000, PR China.
LA  - eng
PT  - Journal Article
DEP - 20170616
PL  - Netherlands
TA  - Gene
JT  - Gene
JID - 7706761
RN  - 0 (Cytokines)
RN  - 0 (NF-kappa B)
RN  - EC 5.2.1.- (Tacrolimus Binding Proteins)
RN  - EC 5.2.1.8 (tacrolimus binding protein 5)
SB  - IM
MH  - Animals
MH  - Cytokines/genetics/*metabolism
MH  - Ganglia, Spinal/cytology/*metabolism
MH  - *Gene Silencing
MH  - Male
MH  - NF-kappa B/*metabolism
MH  - Neuralgia/*genetics/metabolism
MH  - *Pain Threshold
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction
MH  - Tacrolimus Binding Proteins/*genetics/metabolism
MH  - Touch
OTO - NOTNLM
OT  - FKBP51
OT  - NF-kappaB signaling
OT  - Neuro-inflammation
OT  - Neuropathic pain
EDAT- 2017/06/21 06:00
MHDA- 2017/09/19 06:00
CRDT- 2017/06/21 06:00
PHST- 2017/04/17 00:00 [received]
PHST- 2017/06/09 00:00 [revised]
PHST- 2017/06/15 00:00 [accepted]
PHST- 2017/06/21 06:00 [pubmed]
PHST- 2017/09/19 06:00 [medline]
PHST- 2017/06/21 06:00 [entrez]
AID - S0378-1119(17)30479-1 [pii]
AID - 10.1016/j.gene.2017.06.029 [doi]
PST - ppublish
SO  - Gene. 2017 Sep 5;627:169-175. doi: 10.1016/j.gene.2017.06.029. Epub 2017 Jun 16.