Expression of ATF3 and axonal outgrowth are impaired after delayed nerve repair
Saito, Harukazu LU and Dahlin, Lars LU
(2008)
In BMC Neuroscience
9.
- Abstract
- Background: A delay in surgical nerve repair results in impaired nerve function in humans, but mechanisms behind the weakened nerve regeneration are not known. Activating transcription factor 3 (ATF3) increases the intrinsic growth state of injured neurons early after injury, but the role of long-term changes and their relation to axonal outgrowth after a delayed nerve repair are not well understood. ATF3 expression was examined by immunohistochemistry in motor and sensory neurons and in Schwann cells in rat sciatic nerve and related to axonal outgrowth after transection and delayed nerve repair (repair 0, 30, 90 or 180 days post-injury). Expression of the neuronal cell adhesion molecule (NCAM), which is expressed in non-myelinating... (More)
- Background: A delay in surgical nerve repair results in impaired nerve function in humans, but mechanisms behind the weakened nerve regeneration are not known. Activating transcription factor 3 (ATF3) increases the intrinsic growth state of injured neurons early after injury, but the role of long-term changes and their relation to axonal outgrowth after a delayed nerve repair are not well understood. ATF3 expression was examined by immunohistochemistry in motor and sensory neurons and in Schwann cells in rat sciatic nerve and related to axonal outgrowth after transection and delayed nerve repair (repair 0, 30, 90 or 180 days post-injury). Expression of the neuronal cell adhesion molecule (NCAM), which is expressed in non-myelinating Schwann cells, was also examined. Results: The number of neurons and Schwann cells expressing ATF3 declined and the length of axonal outgrowth was impaired if the repair was delayed. The decline was more rapid in motor neurons than in sensory neurons and Schwann cells. Regeneration distances over time correlated to number of ATF3 stained neurons and Schwann cells. Many neurofilament stained axons grew along ATF3 stained Schwann cells. If nerve repair was delayed the majority of Schwann cells in the distal nerve segment stained for NCAM. Conclusion: Delayed nerve repair impairs nerve regeneration and length of axonal outgrowth correlates to ATF3 expression in both neurons and Schwann cells. Mainly non-myelinating Schwann cells (NCAM stained) are present in distal nerve segments after delayed nerve repair. These data provide a neurobiological basis for the poor outcomes associated with delayed nerve repair. Nerve trunks should, if possible, be promptly repaired. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1285866
- author
- Saito, Harukazu
LU
and Dahlin, Lars
LU
- organization
- publishing date
- 2008
- type
- Contribution to journal
- publication status
- published
- subject
- in
- BMC Neuroscience
- volume
- 9
- publisher
- BioMed Central (BMC)
- external identifiers
-
- wos:000259872300001
- scopus:54749154485
- pmid:18801180
- ISSN
- 1471-2202
- DOI
- 10.1186/1471-2202-9-88
- project
- Nerve regeneration - signal transduktion mechanisms, timing and alternatives to nerve grafts
- language
- English
- LU publication?
- yes
- id
- b72bfdd8-6ecc-4cc7-bafc-3ec05e80fa45 (old id 1285866)
- date added to LUP
- 2016-04-01 13:31:39
- date last changed
- 2022-03-21 19:02:52
@article{b72bfdd8-6ecc-4cc7-bafc-3ec05e80fa45,
abstract = {{Background: A delay in surgical nerve repair results in impaired nerve function in humans, but mechanisms behind the weakened nerve regeneration are not known. Activating transcription factor 3 (ATF3) increases the intrinsic growth state of injured neurons early after injury, but the role of long-term changes and their relation to axonal outgrowth after a delayed nerve repair are not well understood. ATF3 expression was examined by immunohistochemistry in motor and sensory neurons and in Schwann cells in rat sciatic nerve and related to axonal outgrowth after transection and delayed nerve repair (repair 0, 30, 90 or 180 days post-injury). Expression of the neuronal cell adhesion molecule (NCAM), which is expressed in non-myelinating Schwann cells, was also examined. Results: The number of neurons and Schwann cells expressing ATF3 declined and the length of axonal outgrowth was impaired if the repair was delayed. The decline was more rapid in motor neurons than in sensory neurons and Schwann cells. Regeneration distances over time correlated to number of ATF3 stained neurons and Schwann cells. Many neurofilament stained axons grew along ATF3 stained Schwann cells. If nerve repair was delayed the majority of Schwann cells in the distal nerve segment stained for NCAM. Conclusion: Delayed nerve repair impairs nerve regeneration and length of axonal outgrowth correlates to ATF3 expression in both neurons and Schwann cells. Mainly non-myelinating Schwann cells (NCAM stained) are present in distal nerve segments after delayed nerve repair. These data provide a neurobiological basis for the poor outcomes associated with delayed nerve repair. Nerve trunks should, if possible, be promptly repaired.}},
author = {{Saito, Harukazu and Dahlin, Lars}},
issn = {{1471-2202}},
language = {{eng}},
publisher = {{BioMed Central (BMC)}},
series = {{BMC Neuroscience}},
title = {{Expression of ATF3 and axonal outgrowth are impaired after delayed nerve repair}},
url = {{http://dx.doi.org/10.1186/1471-2202-9-88}},
doi = {{10.1186/1471-2202-9-88}},
volume = {{9}},
year = {{2008}},
}