PMID- 23456828
OWN - NLM
STAT- MEDLINE
DCOM- 20131030
LR  - 20211203
IS  - 1097-4547 (Electronic)
IS  - 0360-4012 (Linking)
VI  - 91
IP  - 6
DP  - 2013 Jun
TI  - Granulocyte macrophage colony-stimulating factor promotes regeneration of retinal 
      ganglion cells in vitro through a mammalian target of rapamycin-dependent 
      mechanism.
PG  - 771-9
LID - 10.1002/jnr.23205 [doi]
AB  - Lack of regeneration in the adult central nervous system (CNS) is a major hurdle 
      that limits recovery from neurological ailments. Although accumulating research 
      suggests the possibility of axon regeneration by targeting intrinsic signaling 
      mechanisms, it remains a matter of controversy whether functional recovery can be 
      achieved by manipulating aspects of molecular signaling. Recent studies have 
      shown that granulocyte macrophage colony-stimulating factor (GM-CSF) may be an 
      effective means of targeting repair following CNS injury; how this molecule is 
      able to produce this effect is not known. Indeed, GM-CSF has been shown to 
      promote neuronal survival, potentially through activation of as yet unknown 
      cytokine-dependent signals and potentially through regulation of antiapoptotic 
      mechanisms. It is well established that the loss of intrinsic regenerative 
      ability is highly correlated with development of CNS neurons. We therefore 
      designed experiments, using a well-established in vitro retinal ganglion cell 
      (RGC) culture system, to evaluate the effect of GM-CSF on axon growth and cell 
      survival and define possible mechanisms involved in GM-CSF-mediated effects in 
      vitro. Several developmental stages were evaluated, with particular focus placed 
      on stages at which axon growth is known to be significantly diminished. Our 
      results reveal that GM-CSF not only promotes axon growth in postnatal RGCs but 
      also enhances cell survival through a mammalian target of rapamycin 
      (mTOR)-dependent mechanism.
CI  - Copyright (c) 2013 Wiley Periodicals, Inc.
FAU - Legacy, Jacqueline
AU  - Legacy J
AD  - Department of Neuroscience, Carleton University, Ottawa, Ontario, Canada.
FAU - Hanea, Sonia
AU  - Hanea S
FAU - Theoret, Jennifer
AU  - Theoret J
FAU - Smith, Patrice D
AU  - Smith PD
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130304
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/*metabolism/pharmacology
MH  - Immunohistochemistry
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Nerve Regeneration/drug effects/*physiology
MH  - Retinal Ganglion Cells/*cytology/drug effects
MH  - TOR Serine-Threonine Kinases/*metabolism
EDAT- 2013/03/05 06:00
MHDA- 2013/10/31 06:00
CRDT- 2013/03/05 06:00
PHST- 2012/08/28 00:00 [received]
PHST- 2012/11/22 00:00 [revised]
PHST- 2012/12/21 00:00 [accepted]
PHST- 2013/03/05 06:00 [entrez]
PHST- 2013/03/05 06:00 [pubmed]
PHST- 2013/10/31 06:00 [medline]
AID - 10.1002/jnr.23205 [doi]
PST - ppublish
SO  - J Neurosci Res. 2013 Jun;91(6):771-9. doi: 10.1002/jnr.23205. Epub 2013 Mar 4.