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Nerve Injury-Induced c-Jun Activation in Schwann Cells Is JNK Independent.

Lindwall Blom, Charlotta; Mårtensson, Lisa B and Dahlin, Lars LU (2014) In BioMed Research International 2014(Apr 28).
Abstract
We investigated (a) if activation of the mitogen activated protein kinase (MAPK) pathway was linked to the stress activated protein kinase (SAPK) pathway and (b) if JNK was required for activation of c-Jun in Schwann cells of rat sciatic nerve following injury. To this aim, ERK1/2 and the transcription factors c-Jun and ATF-3 were studied by immunohistochemistry in segments of transected nerves. We utilized pharmacological inhibitors of both signal transduction pathways in vitro to determine the effects on downstream signalling events, such as c-Jun activation, and on Schwann cell survival and proliferation. A transection induces c-Jun and ATF-3 transcription in Schwann cells. These events are followed by Schwann cell activation of c-Jun... (More)
We investigated (a) if activation of the mitogen activated protein kinase (MAPK) pathway was linked to the stress activated protein kinase (SAPK) pathway and (b) if JNK was required for activation of c-Jun in Schwann cells of rat sciatic nerve following injury. To this aim, ERK1/2 and the transcription factors c-Jun and ATF-3 were studied by immunohistochemistry in segments of transected nerves. We utilized pharmacological inhibitors of both signal transduction pathways in vitro to determine the effects on downstream signalling events, such as c-Jun activation, and on Schwann cell survival and proliferation. A transection induces c-Jun and ATF-3 transcription in Schwann cells. These events are followed by Schwann cell activation of c-Jun in the injured nerve. The MAPK inhibitor U0126 blocked ERK1/2 activation and reduced Schwann cell proliferation as well as induction of c-Jun transcription. The JNK inhibitor SP600125 reduced Schwann cell proliferation, but did not affect the expression of ERK1/2 or injury-induced increases in c-Jun or ATF-3 levels. Importantly, nerve injury induces Schwann cell activation of c-Jun by phosphorylation, which, in contrast to in sensory neurons, is JNK independent. MAP kinases, other than JNK, can potentially activate c-Jun in Schwann cells following injury; information that is crucial to create new nerve reconstruction strategies. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
BioMed Research International
volume
2014
issue
Apr 28
publisher
Hindawi Publishing Corporation
external identifiers
  • pmid:24877090
  • wos:000335832700001
  • scopus:84925547341
ISSN
2314-6133
DOI
10.1155/2014/392971
language
English
LU publication?
yes
id
ac923011-3629-4450-ac54-d38fa74e8a8e (old id 4452320)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24877090?dopt=Abstract
date added to LUP
2014-06-08 21:21:25
date last changed
2017-10-29 03:16:06
@article{ac923011-3629-4450-ac54-d38fa74e8a8e,
  abstract     = {We investigated (a) if activation of the mitogen activated protein kinase (MAPK) pathway was linked to the stress activated protein kinase (SAPK) pathway and (b) if JNK was required for activation of c-Jun in Schwann cells of rat sciatic nerve following injury. To this aim, ERK1/2 and the transcription factors c-Jun and ATF-3 were studied by immunohistochemistry in segments of transected nerves. We utilized pharmacological inhibitors of both signal transduction pathways in vitro to determine the effects on downstream signalling events, such as c-Jun activation, and on Schwann cell survival and proliferation. A transection induces c-Jun and ATF-3 transcription in Schwann cells. These events are followed by Schwann cell activation of c-Jun in the injured nerve. The MAPK inhibitor U0126 blocked ERK1/2 activation and reduced Schwann cell proliferation as well as induction of c-Jun transcription. The JNK inhibitor SP600125 reduced Schwann cell proliferation, but did not affect the expression of ERK1/2 or injury-induced increases in c-Jun or ATF-3 levels. Importantly, nerve injury induces Schwann cell activation of c-Jun by phosphorylation, which, in contrast to in sensory neurons, is JNK independent. MAP kinases, other than JNK, can potentially activate c-Jun in Schwann cells following injury; information that is crucial to create new nerve reconstruction strategies.},
  articleno    = {392971},
  author       = {Lindwall Blom, Charlotta and Mårtensson, Lisa B and Dahlin, Lars},
  issn         = {2314-6133},
  language     = {eng},
  number       = {Apr 28},
  publisher    = {Hindawi Publishing Corporation},
  series       = {BioMed Research International},
  title        = {Nerve Injury-Induced c-Jun Activation in Schwann Cells Is JNK Independent.},
  url          = {http://dx.doi.org/10.1155/2014/392971},
  volume       = {2014},
  year         = {2014},
}