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Conference Paper: Soluble Nogo66 receptor promotes retinal ganglion cell survival after optic nerve transection and ocular hypertension-induced glaucoma injuries

TitleSoluble Nogo66 receptor promotes retinal ganglion cell survival after optic nerve transection and ocular hypertension-induced glaucoma injuries
Authors
KeywordsNEUROPROTECTION
NOGO
Inhibitory Molecule
Survival
Issue Date2005
PublisherSociety for Neuroscience
Citation
Neuroscience 2005, Washington, DC, 12-16 November 2005, Presentation no. 338.14 How to Cite?
AbstractThree myelin proteins bind to the neuronal Nogo66 receptor (NgR1) that mediates the inhibition of axonal regeneration possibly via two transmembrane coreceptors, LINGO-1 and p75/TROY in the central nervous system (CNS). Modulation of the interactions of these myelin inhibitory proteins with NgR1 can overcome the inhibitory effects of CNS myelin in vitro and in vivo in models of spinal cord injuries. In addition to previous studies that have focused on the roles of NgR1 antagonists in promoting axonal regeneration, here we examined the effect of a soluble fragment of NgR1, sNgR1(27-310)-Fc fusion protein, when injected intravitrealy immediately after injury, on retinal ganglion cell (RGC) survival after ocular hypertension (chronic injury) and optic nerve transection (acute injury). The results showed that sNgR1(27-310)-Fc significantly reduced the loss of RGCs in the ocular hypertension glaucoma model 2 weeks after injury and promoted the survival of RGCs 7 days after optic nerve transection. Thus, sNgR1(27-310)-Fc may exhibit neuroprotective activity in addition to its NgR1 antagonist activity that promotes CNS axonal regeneration. Corresponding authors: KF So and DHS Lee. Supported by Biogen Idec Inc.
Persistent Identifierhttp://hdl.handle.net/10722/95351

 

DC FieldValueLanguage
dc.contributor.authorFu, Qen_HK
dc.contributor.authorChan, SYMen_HK
dc.contributor.authorHu, Ben_HK
dc.contributor.authorWu, Wen_HK
dc.contributor.authorJirik, Aen_HK
dc.contributor.authorLee, Wen_HK
dc.contributor.authorRabacchi, Sen_HK
dc.contributor.authorMi, Sen_HK
dc.contributor.authorSah, DWYen_HK
dc.contributor.authorPepinsky, Ben_HK
dc.contributor.authorLee, DHSen_HK
dc.contributor.authorSo, KFen_HK
dc.date.accessioned2010-09-25T15:59:27Z-
dc.date.available2010-09-25T15:59:27Z-
dc.date.issued2005en_HK
dc.identifier.citationNeuroscience 2005, Washington, DC, 12-16 November 2005, Presentation no. 338.14en_HK
dc.identifier.urihttp://hdl.handle.net/10722/95351-
dc.description.abstractThree myelin proteins bind to the neuronal Nogo66 receptor (NgR1) that mediates the inhibition of axonal regeneration possibly via two transmembrane coreceptors, LINGO-1 and p75/TROY in the central nervous system (CNS). Modulation of the interactions of these myelin inhibitory proteins with NgR1 can overcome the inhibitory effects of CNS myelin in vitro and in vivo in models of spinal cord injuries. In addition to previous studies that have focused on the roles of NgR1 antagonists in promoting axonal regeneration, here we examined the effect of a soluble fragment of NgR1, sNgR1(27-310)-Fc fusion protein, when injected intravitrealy immediately after injury, on retinal ganglion cell (RGC) survival after ocular hypertension (chronic injury) and optic nerve transection (acute injury). The results showed that sNgR1(27-310)-Fc significantly reduced the loss of RGCs in the ocular hypertension glaucoma model 2 weeks after injury and promoted the survival of RGCs 7 days after optic nerve transection. Thus, sNgR1(27-310)-Fc may exhibit neuroprotective activity in addition to its NgR1 antagonist activity that promotes CNS axonal regeneration. Corresponding authors: KF So and DHS Lee. Supported by Biogen Idec Inc.-
dc.languageengen_HK
dc.publisherSociety for Neuroscience-
dc.relation.ispartofSociety for Neuroscience Annual Meetingen_HK
dc.subjectNEUROPROTECTION-
dc.subjectNOGO-
dc.subjectInhibitory Molecule-
dc.subjectSurvival-
dc.titleSoluble Nogo66 receptor promotes retinal ganglion cell survival after optic nerve transection and ocular hypertension-induced glaucoma injuriesen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailChan, SYM: ymchanshirley@yahoo.com.hken_HK
dc.identifier.emailHu, B: bhu@ustc.edu.cnen_HK
dc.identifier.emailWu, W: wtwu@hkucc.hku.hken_HK
dc.identifier.emailSo, KF: hrmaskf@hkucc.hku.hken_HK
dc.identifier.authorityWu, W=rp00419en_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.hkuros112466en_HK

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