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Article: Induction of c-Jun phosphorylation in spinal motoneurons in neonatal and adult rats following axonal injury

TitleInduction of c-Jun phosphorylation in spinal motoneurons in neonatal and adult rats following axonal injury
Authors
Issue Date2010
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainres
Citation
Brain Research, 2010, v. 1320, p. 7-15 How to Cite?
AbstractThis study aims to address if phosphorylation of the transcription factor c-Jun is associated with lesion-induced death of spinal motoneurons, and if this cellular response is modulated by glial-cell-line-derived neurotrophic factor (GDNF). We found that after both distal axotomy and root avulsion, spinal motoneurons in neonatal rats expressed phosphorylated c-Jun (p-c-Jun) and almost all injured motoneurons in these animals died. Similarly, root avulsion in adult rats also induced p-c-Jun expression that preceded the loss of motoneurons. In contrast, neither motoneuron death nor p-c-Jun induction was found after distal axotomy of spinal nerves in adult rats. Application of GDNF after distal axotomy in the neonatal model prevented motoneuron death but did not alter the expression of p-c-Jun in the surviving motoneurons. We conclude that c-Jun phosphorylation correlates with the cellular events leading to motoneuron death and that its expression cannot be modulated by GDNF. We further showed that expression of p-c-Jun was not correlated with the expression of growth-associated protein-43 (GAP-43), whose expression was closely correlated both temporally and spatially with periods of axonal outgrowth, suggesting that p-c-Jun may not be related with axonal regeneration of injured motoneurons. © 2010 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/149732
ISSN
2014 Impact Factor: 2.843
2013 SCImago Journal Rankings: 1.572
ISI Accession Number ID
Funding AgencyGrant Number
HKU Spinal Cord Injury Foundation
University of Hong Kong
Hong Kong Research Grants Council (RGC)
Funding Information:

This study was supported by HKU Spinal Cord Injury Foundation and grants from the University of Hong Kong and Hong Kong Research Grants Council (RGC).

References

 

DC FieldValueLanguage
dc.contributor.authorYuan, Qen_US
dc.contributor.authorHu, Ben_US
dc.contributor.authorWu, Yen_US
dc.contributor.authorChu, THen_US
dc.contributor.authorSu, Hen_US
dc.contributor.authorZhang, Wen_US
dc.contributor.authorSo, KFen_US
dc.contributor.authorLin, Zen_US
dc.contributor.authorWu, Wen_US
dc.date.accessioned2012-06-26T05:57:46Z-
dc.date.available2012-06-26T05:57:46Z-
dc.date.issued2010en_US
dc.identifier.citationBrain Research, 2010, v. 1320, p. 7-15en_US
dc.identifier.issn0006-8993en_US
dc.identifier.urihttp://hdl.handle.net/10722/149732-
dc.description.abstractThis study aims to address if phosphorylation of the transcription factor c-Jun is associated with lesion-induced death of spinal motoneurons, and if this cellular response is modulated by glial-cell-line-derived neurotrophic factor (GDNF). We found that after both distal axotomy and root avulsion, spinal motoneurons in neonatal rats expressed phosphorylated c-Jun (p-c-Jun) and almost all injured motoneurons in these animals died. Similarly, root avulsion in adult rats also induced p-c-Jun expression that preceded the loss of motoneurons. In contrast, neither motoneuron death nor p-c-Jun induction was found after distal axotomy of spinal nerves in adult rats. Application of GDNF after distal axotomy in the neonatal model prevented motoneuron death but did not alter the expression of p-c-Jun in the surviving motoneurons. We conclude that c-Jun phosphorylation correlates with the cellular events leading to motoneuron death and that its expression cannot be modulated by GDNF. We further showed that expression of p-c-Jun was not correlated with the expression of growth-associated protein-43 (GAP-43), whose expression was closely correlated both temporally and spatially with periods of axonal outgrowth, suggesting that p-c-Jun may not be related with axonal regeneration of injured motoneurons. © 2010 Elsevier B.V. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainresen_US
dc.relation.ispartofBrain Researchen_US
dc.subject.meshAging - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnimals, Newbornen_US
dc.subject.meshAxons - Metabolismen_US
dc.subject.meshCell Counten_US
dc.subject.meshCell Death - Physiologyen_US
dc.subject.meshCell Survival - Physiologyen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshFemaleen_US
dc.subject.meshGap-43 Protein - Metabolismen_US
dc.subject.meshGlial Cell Line-Derived Neurotrophic Factor - Metabolismen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshMotor Neurons - Metabolismen_US
dc.subject.meshNerve Regeneration - Physiologyen_US
dc.subject.meshPhosphorylationen_US
dc.subject.meshProto-Oncogene Proteins C-Jun - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshSpinal Cord - Metabolismen_US
dc.subject.meshSpinal Nerves - Injuries - Metabolismen_US
dc.titleInduction of c-Jun phosphorylation in spinal motoneurons in neonatal and adult rats following axonal injuryen_US
dc.typeArticleen_US
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_US
dc.identifier.emailWu, W:wtwu@hkucc.hku.hken_US
dc.identifier.authoritySo, KF=rp00329en_US
dc.identifier.authorityWu, W=rp00419en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.brainres.2010.01.038en_US
dc.identifier.pmid20096669en_US
dc.identifier.scopuseid_2-s2.0-77049119905en_US
dc.identifier.hkuros170571-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77049119905&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume1320en_US
dc.identifier.spage7en_US
dc.identifier.epage15en_US
dc.identifier.isiWOS:000275451000002-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridYuan, Q=7202814773en_US
dc.identifier.scopusauthoridHu, B=35733928400en_US
dc.identifier.scopusauthoridWu, Y=36130811800en_US
dc.identifier.scopusauthoridChu, TH=14023966500en_US
dc.identifier.scopusauthoridSu, H=50162455200en_US
dc.identifier.scopusauthoridZhang, W=50162744600en_US
dc.identifier.scopusauthoridSo, KF=34668391300en_US
dc.identifier.scopusauthoridLin, Z=26433004200en_US
dc.identifier.scopusauthoridWu, W=7407081122en_US

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