PMID- 23681769
OWN - NLM
STAT- MEDLINE
DCOM- 20141023
LR  - 20211203
IS  - 1099-0844 (Electronic)
IS  - 0263-6484 (Linking)
VI  - 32
IP  - 1
DP  - 2014 Jan
TI  - The mechanisms of EGFR in the regulation of axon regeneration.
PG  - 101-5
LID - 10.1002/cbf.2977 [doi]
AB  - To understand the relationship between epidermal growth factor receptor (EGFR) 
      and axon regeneration and the mechanisms of how EGFR regulates the neuronal 
      intrinsic regenerative ability, we evaluated the levels of mRNA and protein of 
      EGFR、total mammalian target of rapamycin (mTOR), p-mTOR(Ser2448) , total Akt and 
      p-Akt(Ser473) in rats of different developmental stage by using Western blot and 
      real-time polymerase chain reaction analysis. Axon protein tau and neuron 
      proteins beta-tubulin/neurofilament (NF) were assessed to evaluate the extent of the 
      axon regeneration in cultured neuron cells. Expressions of EGFR、total mTOR, 
      p-mTOR(Ser2448) , total Akt and p-Akt(Ser473) in cultured neuron cells were also 
      detected using Western blot analysis. Our results showed that the expressions of 
      EGFR and mTOR dropped off with the ageing of the rats, and Ser473 phosphorylation 
      of Akt and Ser2448 phosphorylation of mTOR were highly expressed in foetal and 
      newborn rats but decreased obviously in adult rats. tau, beta-tubulin and NF were 
      upregulated when EGFR was overexpressed and down-regulated after EGFR was 
      blocked. The phosphorylation of mTOR and Akt was apparently elevated when EGFR 
      was overexpressed and decreased when EGFR was blocked, which suggested that EGFR 
      has the potential to regulate the neuronal intrinsic regeneration and mTOR and 
      PI3K/Akt pathway activation may have an important role in it.
CI  - Copyright (c) 2013 John Wiley & Sons, Ltd.
FAU - Xu, Ming-Feng
AU  - Xu MF
AD  - Department of Histology and Embryology, Bethune School of Medical Science, Jilin 
      University, Changchun, 130021, China; Department of physiology, Guangdong Medical 
      College, Dongguan, 523808, China.
FAU - Zhou, Hui
AU  - Zhou H
FAU - Hu, Chuan-Yin
AU  - Hu CY
FAU - Liang, Yan-Qing
AU  - Liang YQ
FAU - Hu, Li
AU  - Hu L
FAU - Chen, Dong
AU  - Chen D
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130517
PL  - England
TA  - Cell Biochem Funct
JT  - Cell biochemistry and function
JID - 8305874
RN  - 0 (RNA, Messenger)
RN  - EC 2.7.1.1 (mTOR protein, rat)
RN  - EC 2.7.10.1 (ErbB Receptors)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Axons/*physiology
MH  - ErbB Receptors/genetics/*metabolism
MH  - Male
MH  - Neurons/physiology
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Spinal Cord/embryology/growth & development/metabolism/pathology
MH  - *Spinal Cord Regeneration
MH  - TOR Serine-Threonine Kinases/genetics/metabolism
OTO - NOTNLM
OT  - EGFR
OT  - PI3K/Akt pathway
OT  - axon regeneration
OT  - mTOR
EDAT- 2013/05/18 06:00
MHDA- 2014/10/24 06:00
CRDT- 2013/05/18 06:00
PHST- 2012/01/22 00:00 [received]
PHST- 2013/03/25 00:00 [revised]
PHST- 2013/04/02 00:00 [accepted]
PHST- 2013/05/18 06:00 [entrez]
PHST- 2013/05/18 06:00 [pubmed]
PHST- 2014/10/24 06:00 [medline]
AID - 10.1002/cbf.2977 [doi]
PST - ppublish
SO  - Cell Biochem Funct. 2014 Jan;32(1):101-5. doi: 10.1002/cbf.2977. Epub 2013 May 
      17.