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Conference Paper: LINGO-1 Antagonists protects retinal ganglion cells in a chronic hypertensive model of glaucoma

TitleLINGO-1 Antagonists protects retinal ganglion cells in a chronic hypertensive model of glaucoma
Authors
Fu, QWu, WHu, BChan, SYMShao, ZPepinsky, RBMi, SSo, KF
Issue Date2006
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neures
Citation
The 29th Annual Meeting of the Japan Neuroscience Society (Neuroscience 2006), Kyoto, Japan, 19–21 July 2006. In Neuroscience Research, 2006, v. 55 n. S1, p. S119 How to Cite?
DOI: http://dx.doi.org/10.1016/j.neures.2006.04.004
AbstractGlaucoma is a progressive neuropathy characterized by loss of vision as a result of retinal ganglion cell (RGC) death. There are no effective neuroprotectants to treat this disorder. LINGO-1 is a member of NgR1-p75/TROY signaling complexes that prevent axonal regeneration in the CNS. We tested the effects of soluble LINGO-1 and anti-LINGO-1 mAb 1A7 on survival of RGCs in the glaucoma model (chronic injury) and optic nerve transection (acute injury). mAb 1A7 significantly reduced the loss of RGCs in the glaucoma model 2 and 4 weeks after injury and also promoted the survival of RGCs after acute injury. Similarly, soluble LINGO-1 improved survival of RGCs in both the chronic and the acute injury models. Consistent with the effect on survival, soluble LINGO-1 induced Akt activation in vivo. These results indicate that LINGO-1 antagonists have potential therapeutic applications to treat glaucoma.
Persistent Identifierhttp://hdl.handle.net/10722/95044
ISSN
0168-0102
2023 Impact Factor: 2.4
2023 SCImago Journal Rankings: 0.811
ISI Accession Number ID
WOS:000238609700002

 

DC FieldValueLanguage
dc.contributor.authorFu, Qen_HK
dc.contributor.authorWu, Wen_HK
dc.contributor.authorHu, Ben_HK
dc.contributor.authorChan, SYMen_HK
dc.contributor.authorShao, Zen_HK
dc.contributor.authorPepinsky, RBen_HK
dc.contributor.authorMi, Sen_HK
dc.contributor.authorSo, KFen_HK
dc.date.accessioned2010-09-25T15:49:53Z-
dc.date.available2010-09-25T15:49:53Z-
dc.date.issued2006en_HK
dc.identifier.citationThe 29th Annual Meeting of the Japan Neuroscience Society (Neuroscience 2006), Kyoto, Japan, 19–21 July 2006. In Neuroscience Research, 2006, v. 55 n. S1, p. S119en_HK
dc.identifier.issn0168-0102-
dc.identifier.urihttp://hdl.handle.net/10722/95044-
dc.description.abstractGlaucoma is a progressive neuropathy characterized by loss of vision as a result of retinal ganglion cell (RGC) death. There are no effective neuroprotectants to treat this disorder. LINGO-1 is a member of NgR1-p75/TROY signaling complexes that prevent axonal regeneration in the CNS. We tested the effects of soluble LINGO-1 and anti-LINGO-1 mAb 1A7 on survival of RGCs in the glaucoma model (chronic injury) and optic nerve transection (acute injury). mAb 1A7 significantly reduced the loss of RGCs in the glaucoma model 2 and 4 weeks after injury and also promoted the survival of RGCs after acute injury. Similarly, soluble LINGO-1 improved survival of RGCs in both the chronic and the acute injury models. Consistent with the effect on survival, soluble LINGO-1 induced Akt activation in vivo. These results indicate that LINGO-1 antagonists have potential therapeutic applications to treat glaucoma.-
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neures-
dc.relation.ispartofNeuroscience Researchen_HK
dc.titleLINGO-1 Antagonists protects retinal ganglion cells in a chronic hypertensive model of glaucomaen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailWu, W: wtwu@hkucc.hku.hken_HK
dc.identifier.emailHu, B: bhu@ustc.edu.cnen_HK
dc.identifier.emailChan, SYM: ymchanshirley@yahoo.com.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.doi10.1016/j.neures.2006.04.004-
dc.identifier.scopuseid_2-s2.0-33746074496-
dc.identifier.hkuros125796en_HK
dc.identifier.spageS119en_HK
dc.identifier.epageS119en_HK
dc.identifier.isiWOS:000238609700002-
dc.identifier.issnl0168-0102-

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