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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4452320
- author
- Lindwall Blom, Charlotta
; Mårtensson, Lisa B
and Dahlin, Lars
LU
- organization
- publishing date
- 2014
- type
- Contribution to journal
- publication status
- published
- subject
- in
- BioMed Research International
- volume
- 2014
- issue
- Apr 28
- article number
- 392971
- publisher
- Hindawi Limited
- external identifiers
-
- pmid:24877090
- wos:000335832700001
- pmid:24877090
- scopus:84901253725
- 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
- 2016-04-01 10:45:21
- date last changed
- 2022-01-26 02:09:47
@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.}},
author = {{Lindwall Blom, Charlotta and Mårtensson, Lisa B and Dahlin, Lars}},
issn = {{2314-6133}},
language = {{eng}},
number = {{Apr 28}},
publisher = {{Hindawi Limited}},
series = {{BioMed Research International}},
title = {{Nerve Injury-Induced c-Jun Activation in Schwann Cells Is JNK Independent.}},
url = {{https://lup.lub.lu.se/search/files/2108872/4986304.pdf}},
doi = {{10.1155/2014/392971}},
volume = {{2014}},
year = {{2014}},
}