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Article: Decreased c-Jun expression correlates with impaired spinal motoneuron regeneration in aged mice following sciatic nerve crush

TitleDecreased c-Jun expression correlates with impaired spinal motoneuron regeneration in aged mice following sciatic nerve crush
Authors
KeywordsAging
Axonal injury
Axonal regeneration
Motoneuron
Mouse
Transcription factor
Issue Date2012
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/expgero
Citation
Experimental Gerontology, 2012, v. 47 n. 4, p. 329-336 How to Cite?
Abstract
Post-injury nerve regeneration of the peripheral nervous system declines with age, but the mechanisms underlying the weakened axonal regeneration are not well understood. Increased synthesis and activity of the AP-1 transcription factor c-Jun have been implicated in efficient motor axonal regeneration. In the present study, we evaluated the hypothesis that the impaired regenerative capacity in the aged is associated with impaired induction of c-Jun. In non-manipulated young adult or aged mice, no c-Jun and its phosphorylated form were detected in the ventral horn of the spinal cord. Following nerve crush, significant c-Jun and phosphorylated c-Jun occurred in the injured motoneurons of young adult mice, but not in aged animals. In accord with the immunohistochemistry, Western blots also showed that sciatic nerve crush induced c-Jun and its phosphorylation expression in the ventral horn of young adult but not in aged mice. Changes in c-Jun mRNA level detected by in situ hybridization are congruent with that in c-Jun protein content, showing an increase at 5. days after crush in young adult but not aged. Moreover, compared with young adult mice, aged mice showed impaired motor axonal regeneration. These results demonstrate that the impaired motor axonal regeneration seen in aged mice is correlated with impaired c-Jun expression and phosphorylation following injury. These data provide a neurobiological explanation for the poor outcome associated with nerve repair in the aged. © 2012 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/147661
ISSN
2013 Impact Factor: 3.529
2013 SCImago Journal Rankings: 1.592
ISI Accession Number ID
Funding AgencyGrant Number
Chinese University of Hong Kong
University of Hong Kong
National Basic Research Program of China (973 program)2011CB504402
Hong Universities Grant CouncilAoE/M-04/04
Funding Information:

This study was supported by the Chinese University of Hong Kong, the University of Hong Kong and the National Basic Research Program of China (973 program; 2011CB504402). KY Tsang and KSE Cheah are supported by Hong Universities Grant Council project AoE/M-04/04. We thank Dr. IC Bruce of Zhejiang University School of Medicine for reading the manuscript.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorYuan, Qen_HK
dc.contributor.authorSu, Hen_HK
dc.contributor.authorGuo, Jen_HK
dc.contributor.authorTsang, KYen_HK
dc.contributor.authorCheah, KSEen_HK
dc.contributor.authorChiu, Ken_HK
dc.contributor.authorYang, Jen_HK
dc.contributor.authorWong, WMen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorHuang, JDen_HK
dc.contributor.authorWu, Wen_HK
dc.contributor.authorLin, ZXen_HK
dc.date.accessioned2012-05-29T06:05:20Z-
dc.date.available2012-05-29T06:05:20Z-
dc.date.issued2012en_HK
dc.identifier.citationExperimental Gerontology, 2012, v. 47 n. 4, p. 329-336en_HK
dc.identifier.issn0531-5565en_HK
dc.identifier.urihttp://hdl.handle.net/10722/147661-
dc.description.abstractPost-injury nerve regeneration of the peripheral nervous system declines with age, but the mechanisms underlying the weakened axonal regeneration are not well understood. Increased synthesis and activity of the AP-1 transcription factor c-Jun have been implicated in efficient motor axonal regeneration. In the present study, we evaluated the hypothesis that the impaired regenerative capacity in the aged is associated with impaired induction of c-Jun. In non-manipulated young adult or aged mice, no c-Jun and its phosphorylated form were detected in the ventral horn of the spinal cord. Following nerve crush, significant c-Jun and phosphorylated c-Jun occurred in the injured motoneurons of young adult mice, but not in aged animals. In accord with the immunohistochemistry, Western blots also showed that sciatic nerve crush induced c-Jun and its phosphorylation expression in the ventral horn of young adult but not in aged mice. Changes in c-Jun mRNA level detected by in situ hybridization are congruent with that in c-Jun protein content, showing an increase at 5. days after crush in young adult but not aged. Moreover, compared with young adult mice, aged mice showed impaired motor axonal regeneration. These results demonstrate that the impaired motor axonal regeneration seen in aged mice is correlated with impaired c-Jun expression and phosphorylation following injury. These data provide a neurobiological explanation for the poor outcome associated with nerve repair in the aged. © 2012 Elsevier Inc.en_HK
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/expgeroen_HK
dc.relation.ispartofExperimental Gerontologyen_HK
dc.subjectAgingen_HK
dc.subjectAxonal injuryen_HK
dc.subjectAxonal regenerationen_HK
dc.subjectMotoneuronen_HK
dc.subjectMouseen_HK
dc.subjectTranscription factoren_HK
dc.titleDecreased c-Jun expression correlates with impaired spinal motoneuron regeneration in aged mice following sciatic nerve crushen_HK
dc.typeArticleen_HK
dc.identifier.emailCheah, KSE:hrmbdkc@hku.hken_HK
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_HK
dc.identifier.emailWu, W:wtwu@hkucc.hku.hken_HK
dc.identifier.authorityCheah, KSE=rp00342en_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityHuang, JD=rp00451en_HK
dc.identifier.authorityWu, W=rp00419-
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.exger.2012.02.006en_HK
dc.identifier.pmid22382134-
dc.identifier.scopuseid_2-s2.0-84862829326-
dc.identifier.hkuros199492-
dc.identifier.hkuros210513-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84858440420&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume47en_HK
dc.identifier.issue4en_HK
dc.identifier.spage329en_HK
dc.identifier.epage336en_HK
dc.identifier.isiWOS:000302624500007-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectDevelopmental genomics and skeletal research-
dc.identifier.scopusauthoridYuan, Q=7202814773en_HK
dc.identifier.scopusauthoridSu, H=16317750200en_HK
dc.identifier.scopusauthoridGuo, J=55049464800en_HK
dc.identifier.scopusauthoridTsang, KY=55048261100en_HK
dc.identifier.scopusauthoridCheah, KSE=35387746200en_HK
dc.identifier.scopusauthoridChiu, K=15076970500en_HK
dc.identifier.scopusauthoridYang, J=55054236700en_HK
dc.identifier.scopusauthoridWong, WM=55054360500en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK
dc.identifier.scopusauthoridHuang, JD=55055682100en_HK
dc.identifier.scopusauthoridWu, W=7407081122en_HK
dc.identifier.scopusauthoridLin, ZX=26433004200en_HK
dc.identifier.citeulike10397378-

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