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Conference Paper: Delayed activation of caspase-3 in response to cytochrome c release in axotomized retinal ganglion cells

TitleDelayed activation of caspase-3 in response to cytochrome c release in axotomized retinal ganglion cells
Authors
Keywordsapoptosis
axotomy
nerve injury
neuronal death
Issue Date2001
PublisherSociety for Neuroscience.
Citation
The 31st Annual Meeting of Society for Neuroscience (Neuroscience 2001), San Diego, CA., 10–15 November 2001. How to Cite?
AbstractTransection of the optic nerve results in delayed death of axotomized retinal ganglion cells (RGCs). While activation of caspase-3 and -9 has been implicated in axotomized RGC death, the upstream pathways involved in the activation of these caspases remain unknown. Since cytochrome c release from the mitochondria can lead to activation of casapse-9 and subsequently caspase-3, we hypothesize that cytochrome c release is involved in the initiation of apoptosis in axotomized RGCs. In adult hamsters, incidence of cytochrome c release, activation of caspase-3 and nuclear fragmentation were quantified at different time-points following optic nerve transection using immunohistochemistry. We found that cytochrome c release was observed at 1 day post-axotomy (dpa). Cytochrome c immunoreactivity localized entirely to the ganglion cell layer (GCL) and almost exclusively to Fluoro-Gold-labeled RGCs. This suggests that the cytochrome c release observed is injury-related. Activation of caspase-3 and nuclear fragmentation were first observed at 3 dpa. The activation of caspase-3 coincided with the beginning of axotomized RGC loss and was again observed only in the GCL. Our data suggest that cytochrome c release may be implicated in the activation of caspase-3 in axotomized RGCs. Activation of caspase-3 was delayed by two days after cytochrome c release. The delayed activation of caspase-3 suggests that the apoptotic cascade initiated after axotomy may be halted at a site downstream of cytochrome c release but upstream of caspase-3 activation. This observation may account for the delayed death of RGCs after axotomy in adult hamsters. Supported by An award from the University of Hong Kong
DescriptionPresentation no. 870.1
Persistent Identifierhttp://hdl.handle.net/10722/95096

 

DC FieldValueLanguage
dc.contributor.authorCheung, HYZen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorYip, HKFen_HK
dc.contributor.authorWu, Wen_HK
dc.date.accessioned2010-09-25T15:51:31Z-
dc.date.available2010-09-25T15:51:31Z-
dc.date.issued2001en_HK
dc.identifier.citationThe 31st Annual Meeting of Society for Neuroscience (Neuroscience 2001), San Diego, CA., 10–15 November 2001.-
dc.identifier.urihttp://hdl.handle.net/10722/95096-
dc.descriptionPresentation no. 870.1-
dc.description.abstractTransection of the optic nerve results in delayed death of axotomized retinal ganglion cells (RGCs). While activation of caspase-3 and -9 has been implicated in axotomized RGC death, the upstream pathways involved in the activation of these caspases remain unknown. Since cytochrome c release from the mitochondria can lead to activation of casapse-9 and subsequently caspase-3, we hypothesize that cytochrome c release is involved in the initiation of apoptosis in axotomized RGCs. In adult hamsters, incidence of cytochrome c release, activation of caspase-3 and nuclear fragmentation were quantified at different time-points following optic nerve transection using immunohistochemistry. We found that cytochrome c release was observed at 1 day post-axotomy (dpa). Cytochrome c immunoreactivity localized entirely to the ganglion cell layer (GCL) and almost exclusively to Fluoro-Gold-labeled RGCs. This suggests that the cytochrome c release observed is injury-related. Activation of caspase-3 and nuclear fragmentation were first observed at 3 dpa. The activation of caspase-3 coincided with the beginning of axotomized RGC loss and was again observed only in the GCL. Our data suggest that cytochrome c release may be implicated in the activation of caspase-3 in axotomized RGCs. Activation of caspase-3 was delayed by two days after cytochrome c release. The delayed activation of caspase-3 suggests that the apoptotic cascade initiated after axotomy may be halted at a site downstream of cytochrome c release but upstream of caspase-3 activation. This observation may account for the delayed death of RGCs after axotomy in adult hamsters. Supported by An award from the University of Hong Kong-
dc.languageengen_HK
dc.publisherSociety for Neuroscience.-
dc.relation.ispartofNeuroscience 2001en_HK
dc.subjectapoptosis-
dc.subjectaxotomy-
dc.subjectnerve injury-
dc.subjectneuronal death-
dc.titleDelayed activation of caspase-3 in response to cytochrome c release in axotomized retinal ganglion cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailSo, KF: hrmaskf@hkucc.hku.hken_HK
dc.identifier.emailYip, HKF: hkfyip@hku.hken_HK
dc.identifier.emailWu, W: wtwu@hkucc.hku.hken_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityWu, W=rp00419en_HK
dc.identifier.hkuros109273en_HK

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