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Article: Regulation of caspase activation in axotomized retinal ganglion cells

TitleRegulation of caspase activation in axotomized retinal ganglion cells
Authors
Issue Date2004
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ymcne
Citation
Molecular And Cellular Neuroscience, 2004, v. 25 n. 3, p. 383-393 How to Cite?
AbstractTransection of the optic nerve initiates massive death of retinal ganglion cells (RGCs). Interestingly, despite the severity of the injury, RGC loss was not observed until several days after axotomy. The mechanisms responsible for this initial lack of RGC death remained unknown. In the current study, immunohistochemical analysis revealed that caspases-3 and -9 activation in the RGCs were not detected until day 3 post-axotomy, coinciding with the onset of axotomy-induced RGC loss. Interestingly, elevated Akt phosphorylation was observed in axotomized retinas during the absence of caspase activation. Inhibiting the increase in Akt phosphorylation by intravitreal injection of wortmannin and LY294002, inhibitors of PI3K, resulted in premature nuclear fragmentation, caspases-3 and -9 activation in the ganglion cell layer. Our findings thus indicate that the PI3K/Akt pathway may serve as an endogenous regulator of caspase activation in axotomized RGCs, thereby, contributing to the late onset of RGC death following axotomy. © 2004 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67651
ISSN
2015 Impact Factor: 3.597
2015 SCImago Journal Rankings: 2.342
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, ZHen_HK
dc.contributor.authorChan, YMen_HK
dc.contributor.authorSiu, FKWen_HK
dc.contributor.authorYip, HKen_HK
dc.contributor.authorWu, Wen_HK
dc.contributor.authorLeung, MCPen_HK
dc.contributor.authorSo, KFen_HK
dc.date.accessioned2010-09-06T05:57:02Z-
dc.date.available2010-09-06T05:57:02Z-
dc.date.issued2004en_HK
dc.identifier.citationMolecular And Cellular Neuroscience, 2004, v. 25 n. 3, p. 383-393en_HK
dc.identifier.issn1044-7431en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67651-
dc.description.abstractTransection of the optic nerve initiates massive death of retinal ganglion cells (RGCs). Interestingly, despite the severity of the injury, RGC loss was not observed until several days after axotomy. The mechanisms responsible for this initial lack of RGC death remained unknown. In the current study, immunohistochemical analysis revealed that caspases-3 and -9 activation in the RGCs were not detected until day 3 post-axotomy, coinciding with the onset of axotomy-induced RGC loss. Interestingly, elevated Akt phosphorylation was observed in axotomized retinas during the absence of caspase activation. Inhibiting the increase in Akt phosphorylation by intravitreal injection of wortmannin and LY294002, inhibitors of PI3K, resulted in premature nuclear fragmentation, caspases-3 and -9 activation in the ganglion cell layer. Our findings thus indicate that the PI3K/Akt pathway may serve as an endogenous regulator of caspase activation in axotomized RGCs, thereby, contributing to the late onset of RGC death following axotomy. © 2004 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ymcneen_HK
dc.relation.ispartofMolecular and Cellular Neuroscienceen_HK
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in Molecular and Cellular Neuroscience. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Molecular and Cellular Neuroscience, [VOL 25, ISSUE 3, 2004] DOI 10.1016/j.mcn.2003.11.001-
dc.subject.meshCaspases - metabolism-
dc.subject.meshEnzyme Activation - drug effects - physiology-
dc.subject.meshEnzyme Inhibitors - pharmacology-
dc.subject.meshOptic Nerve Injuries - enzymology-
dc.subject.meshRetinal Ganglion Cells - drug effects - enzymology-
dc.titleRegulation of caspase activation in axotomized retinal ganglion cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailCheung, ZH:zelda@hku.hken_HK
dc.identifier.emailYip, HK:hkfyip@hku.hken_HK
dc.identifier.emailWu, W:wtwu@hkucc.hku.hken_HK
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_HK
dc.identifier.authorityCheung, ZH=rp01588en_HK
dc.identifier.authorityYip, HK=rp00285en_HK
dc.identifier.authorityWu, W=rp00419en_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.mcn.2003.11.001en_HK
dc.identifier.pmid15033167-
dc.identifier.scopuseid_2-s2.0-1642305636en_HK
dc.identifier.hkuros86039en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1642305636&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume25en_HK
dc.identifier.issue3en_HK
dc.identifier.spage383en_HK
dc.identifier.epage393en_HK
dc.identifier.isiWOS:000220581600004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheung, ZH=6507483375en_HK
dc.identifier.scopusauthoridChan, YM=36989085800en_HK
dc.identifier.scopusauthoridSiu, FKW=6701518486en_HK
dc.identifier.scopusauthoridYip, HK=7101980864en_HK
dc.identifier.scopusauthoridWu, W=7407081122en_HK
dc.identifier.scopusauthoridLeung, MCP=7201943351en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK

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