PMID- 24753179
OWN - NLM
STAT- MEDLINE
DCOM- 20150102
LR  - 20140513
IS  - 1097-4547 (Electronic)
IS  - 0360-4012 (Linking)
VI  - 92
IP  - 7
DP  - 2014 Jul
TI  - Electrically induced brain-derived neurotrophic factor release from Schwann 
      cells.
PG  - 893-903
LID - 10.1002/jnr.23365 [doi]
AB  - Regulating the production of brain-derived neurotrophic factor (BDNF) in Schwann 
      cells (SCs) is critical for their application in traumatic nerve injury, 
      neurodegenerative disorders, and demyelination disease in both central and 
      peripheral nervous systems. The present study investigated the possibility of 
      using electrical stimulation (ES) to activate SCs to release BDNF. We found that 
      short-term ES was capable of promoting BDNF production from SCs, and the maximal 
      BDNF release was achieved by ES at 6 V (3 Hz, 30 min). We further examined the 
      involvement of intracellular calcium ions ([Ca2+]i) in the ES-induced BDNF 
      production in SCs by pharmacological studies. We found that the ES-induced BDNF 
      release required calcium influx through T-type voltage-gated calcium channel 
      (VGCC) and calcium mobilization from internal calcium stores, including inositol 
      triphosphate-sensitive stores and caffeine/ryanodine-sensitive stores. In 
      addition, calcium-calmodulin dependent protein kinase IV (CaMK IV), 
      mitogen-activated protein kinase (MAPK), and cAMP response element-binding 
      protein (CREB) were found to play important roles in the ES-induced BDNF release 
      from SCs. In conclusion, ES is capable of activating SCs to secrete BDNF, which 
      requires the involvement of calcium influx through T-type VGCC and calcium 
      mobilization from internal calcium stores. In addition, activation of CaMK IV, 
      MAPK, and CREB were also involved in the ES-induced BDNF release. The findings 
      indicate that ES can improve the neurotrophic ability in SCs and raise the 
      possibility of developing electrically stimulated SCs as a source of cell therapy 
      for nerve injury in both peripheral and central nervous systems.
CI  - Copyright (c) 2014 Wiley Periodicals, Inc.
FAU - Luo, Beier
AU  - Luo B
AD  - Institute of Orthopaedics, Changhai Hospital, The Second Military Medical 
      University, Shanghai, China.
FAU - Huang, Jinghui
AU  - Huang J
FAU - Lu, Lei
AU  - Lu L
FAU - Hu, Xueyu
AU  - Hu X
FAU - Luo, Zhuojing
AU  - Luo Z
FAU - Li, Ming
AU  - Li M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140219
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (S100 Proteins)
RN  - EC 2.3.1.48 (CREB-Binding Protein)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 4)
RN  - M03GIQ7Z6P (Sincalide)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Brachial Plexus/cytology
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - CREB-Binding Protein/metabolism
MH  - Calcium/metabolism
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 4/metabolism
MH  - Cell Count
MH  - Cell Proliferation
MH  - Cell Survival
MH  - Cells, Cultured
MH  - Electric Stimulation/*methods
MH  - Enzyme Inhibitors/pharmacology
MH  - RNA, Small Interfering/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - S100 Proteins/metabolism
MH  - Schwann Cells/*metabolism
MH  - Sciatic Nerve/cytology
MH  - Sincalide/metabolism
OTO - NOTNLM
OT  - brain-derived neurotrophic factor
OT  - calcium
OT  - calcium-calmodulin dependent protein kinase
OT  - electrical stimulation
OT  - mitogen-activated protein kinase
EDAT- 2014/04/23 06:00
MHDA- 2015/01/03 06:00
CRDT- 2014/04/23 06:00
PHST- 2013/07/03 00:00 [received]
PHST- 2013/12/18 00:00 [revised]
PHST- 2013/12/27 00:00 [accepted]
PHST- 2014/04/23 06:00 [entrez]
PHST- 2014/04/23 06:00 [pubmed]
PHST- 2015/01/03 06:00 [medline]
AID - 10.1002/jnr.23365 [doi]
PST - ppublish
SO  - J Neurosci Res. 2014 Jul;92(7):893-903. doi: 10.1002/jnr.23365. Epub 2014 Feb 19.