PMID- 22552324
OWN - NLM
STAT- MEDLINE
DCOM- 20120910
LR  - 20220409
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Linking)
VI  - 6
IP  - 1
DP  - 2012 Jul
TI  - High glucose levels increase the expression of neurotrophic factors associated 
      with p-p42/p44 MAPK in Schwann cells in vitro.
PG  - 179-84
LID - 10.3892/mmr.2012.896 [doi]
AB  - Diabetic peripheral neuropathy (DPN) is one of the most common complications of 
      diabetes mellitus. One contributing factor to DPN is altered neurotrophism due to 
      changes in the synthesis and expression of neurotrophins. Schwann cells (SCs) are 
      the myelin-forming cells of the peripheral nervous system that promote nerve 
      regeneration through the expression and secretion of neurotrophic factors (NTFs). 
      Therefore, in this study, using SCs cultured in the presence of high levels of 
      glucose for 24 h, with and without the p42/p44 mitogen-activated protein kinase 
      (MAPK) inhibitor, PD98059, we investigated the effect of high glucose levels on 
      SCs over a short period of time. The cultured cells were evaluated using 
      3(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide (MTT) assay, Hoechst 
      staining, immunocytochemistry, reverse transcriptase-polymerase chain reaction 
      and western blot analysis. High glucose levels did not promote morphological 
      abnormalities or decrease the viability of SCs. However, high glucose levels 
      enhanced the expression of nerve growth factor (NGF) and brain-derived 
      neurotrophic factor (BDNF) and induced the activation of p42/p44 MAPK in cultured 
      SCs in a dose-dependent manner. Additionally, the phosphorylation of p42/p44 MAPK 
      may be associated with the expression of NTFs by SCs exposed to high glucose 
      conditions; the excessive activation of p42/p44 MAPK inhibited the expression of 
      NTFs. These observations demonstrate that exposure to high glucose levels lead to 
      acutely elevated levels of NGF and BDNF in SCs over a short period of time, which 
      may be involved in the p42/p44 MAPK pathway.
FAU - Zhu, Hao
AU  - Zhu H
AD  - Department of Anatomy, Shanghai Jiao Tong University School of Medicine, 
      Shanghai, PR China.
FAU - Yu, Wen-Juan
AU  - Yu WJ
FAU - Le, Yan
AU  - Le Y
FAU - Wang, Wen-Jin
AU  - Wang WJ
FAU - Li, Feng
AU  - Li F
FAU - Gui, Ting
AU  - Gui T
FAU - Wang, Yue-Ming
AU  - Wang YM
FAU - Shi, Wo-Dong
AU  - Shi WD
FAU - Ding, Wen-Long
AU  - Ding WL
FAU - Fan, Xian-Qun
AU  - Fan XQ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120502
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (Nerve Growth Factors)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Enzyme Activation/drug effects
MH  - *Gene Expression Regulation/drug effects
MH  - Glucose/*metabolism/pharmacology
MH  - Humans
MH  - MAP Kinase Signaling System/drug effects
MH  - Mitogen-Activated Protein Kinase 1/*metabolism
MH  - Mitogen-Activated Protein Kinase 3/*metabolism
MH  - Nerve Growth Factors/*genetics/metabolism
MH  - Phosphorylation/drug effects
MH  - Schwann Cells/cytology/drug effects/*metabolism
MH  - Transcription, Genetic/drug effects
MH  - Up-Regulation/drug effects/genetics
OTO - NOTNLM
OT  - Schwann cell
OT  - high glucose
OT  - neurotrophic factors
OT  - p42/p44 mitogen-activated protein kinase
EDAT- 2012/05/04 06:00
MHDA- 2012/09/11 06:00
CRDT- 2012/05/04 06:00
PHST- 2012/01/11 00:00 [received]
PHST- 2012/04/12 00:00 [accepted]
PHST- 2012/05/04 06:00 [entrez]
PHST- 2012/05/04 06:00 [pubmed]
PHST- 2012/09/11 06:00 [medline]
AID - 10.3892/mmr.2012.896 [doi]
PST - ppublish
SO  - Mol Med Rep. 2012 Jul;6(1):179-84. doi: 10.3892/mmr.2012.896. Epub 2012 May 2.