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Article: Soluble Nogo-66 receptor prevents synaptic dysfunction and rescues retinal ganglion cell loss in chronic glaucoma.

TitleSoluble Nogo-66 receptor prevents synaptic dysfunction and rescues retinal ganglion cell loss in chronic glaucoma.
Authors
Issue Date2011
PublisherAssociation for Research in Vision and Ophthalmology. The Journal's web site is located at http://www.iovs.org
Citation
Investigative Ophthalmology & Visual Science, 2011, v. 52 n. 11, p. 8374-8380 How to Cite?
AbstractMyelin inhibitory proteins inhibit axon growth and synaptic function by binding to the Nogo-66 receptor (NgR)1 in the central nervous system. Glaucoma is a progressive neuropathy characterized by loss of vision as a result of retinal ganglion cell (RGC) death. Synaptic degeneration is thought to be an early pathology of neurodegeneration in glaucoma and precedes RGC loss. The authors aimed to examine whether the NgR1 antagonist promotes synaptic recovery and RGC survival in glaucoma. Experimental ocular hypertension model was induced in adult rats with laser coagulation of the episcleral and limbal veins. NgR1 antagonist, soluble NgR1 (sNgR-Fc) was administrated to examine their effect on synaptic recovery and RGC survival. Expression of c-Fos, a neuronal connectivity marker, in the retinas was investigated using immunohistochemistry. NgR1 was expressed in RGCs and upregulated after intraocular pressure elevation. Treatment with sNgR-Fc significantly reduced RGC loss at 2 and 4 weeks after the induction of ocular hypertension and also promoted RGC survival after optic nerve transection. There was no RGC loss at 5 days but there was significant synaptic degeneration as measured by c-Fos. Administration of sNgR-Fc attenuated synaptic degeneration at 5 days, and at 2 and 4 weeks. These data suggest that synaptic degeneration may be an initial molecular mechanism for neurodegeneration in glaucoma and appropriate NgR1 antagonism may delay the progression of the disease.
Persistent Identifierhttp://hdl.handle.net/10722/146838
ISSN
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong Kong
NSFC30801272
81071030
81170896
Science and Technology Foundation of Guangdong Province, China2008B030301090
2010B031600089
2011B031800243
RFDP200805581160
Fundamental Research Funds for the Central Universities09ykpy25
09ykpy31
National Basic Research Program of China (973 Program)2011CB707501
Funding Information:

Supported by funding from the Jessie Ho Professorship in Neurosciences from the University of Hong Kong, NSFC (30801272, 81071030, 81170896); Science and Technology Foundation of Guangdong Province, China (2008B030301090, 2010B031600089, 2011B031800243), RFDP (200805581160); the Fundamental Research Funds for the Central Universities (09ykpy25, 09ykpy31); and National Basic Research Program of China (973 Program) (2011CB707501).

 

DC FieldValueLanguage
dc.contributor.authorFu, QLen_HK
dc.contributor.authorLiao, XXen_HK
dc.contributor.authorLi, Xen_HK
dc.contributor.authorChen, Den_HK
dc.contributor.authorShi, Jen_HK
dc.contributor.authorWen, Wen_HK
dc.contributor.authorLee, DHen_HK
dc.contributor.authorSo, KFen_HK
dc.date.accessioned2012-05-23T05:42:27Z-
dc.date.available2012-05-23T05:42:27Z-
dc.date.issued2011en_HK
dc.identifier.citationInvestigative Ophthalmology & Visual Science, 2011, v. 52 n. 11, p. 8374-8380en_HK
dc.identifier.issn1552-5783en_HK
dc.identifier.urihttp://hdl.handle.net/10722/146838-
dc.description.abstractMyelin inhibitory proteins inhibit axon growth and synaptic function by binding to the Nogo-66 receptor (NgR)1 in the central nervous system. Glaucoma is a progressive neuropathy characterized by loss of vision as a result of retinal ganglion cell (RGC) death. Synaptic degeneration is thought to be an early pathology of neurodegeneration in glaucoma and precedes RGC loss. The authors aimed to examine whether the NgR1 antagonist promotes synaptic recovery and RGC survival in glaucoma. Experimental ocular hypertension model was induced in adult rats with laser coagulation of the episcleral and limbal veins. NgR1 antagonist, soluble NgR1 (sNgR-Fc) was administrated to examine their effect on synaptic recovery and RGC survival. Expression of c-Fos, a neuronal connectivity marker, in the retinas was investigated using immunohistochemistry. NgR1 was expressed in RGCs and upregulated after intraocular pressure elevation. Treatment with sNgR-Fc significantly reduced RGC loss at 2 and 4 weeks after the induction of ocular hypertension and also promoted RGC survival after optic nerve transection. There was no RGC loss at 5 days but there was significant synaptic degeneration as measured by c-Fos. Administration of sNgR-Fc attenuated synaptic degeneration at 5 days, and at 2 and 4 weeks. These data suggest that synaptic degeneration may be an initial molecular mechanism for neurodegeneration in glaucoma and appropriate NgR1 antagonism may delay the progression of the disease.en_HK
dc.languageengen_US
dc.publisherAssociation for Research in Vision and Ophthalmology. The Journal's web site is located at http://www.iovs.orgen_US
dc.relation.ispartofInvestigative ophthalmology & visual scienceen_HK
dc.subject.meshGlaucoma - metabolism - pathology - prevention and control-
dc.subject.meshMyelin Proteins - antagonists and inhibitors - physiology-
dc.subject.meshNerve Degeneration - metabolism - pathology - prevention and control-
dc.subject.meshReceptors, Cell Surface - antagonists and inhibitors - physiology-
dc.subject.meshRecombinant Fusion Proteins - administration and dosage-
dc.titleSoluble Nogo-66 receptor prevents synaptic dysfunction and rescues retinal ganglion cell loss in chronic glaucoma.en_HK
dc.typeArticleen_HK
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1167/iovs.11-7667-
dc.identifier.pmid21948553en_HK
dc.identifier.scopuseid_2-s2.0-84855375934en_HK
dc.identifier.hkuros199488en_US
dc.identifier.hkuros197907en_US
dc.identifier.volume52en_HK
dc.identifier.issue11en_HK
dc.identifier.spage8374en_HK
dc.identifier.epage8380en_HK
dc.identifier.isiWOS:000296907700019-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridFu, QL=23388762000en_HK
dc.identifier.scopusauthoridLiao, XX=54398828500en_HK
dc.identifier.scopusauthoridLi, X=54882957300en_HK
dc.identifier.scopusauthoridChen, D=54883825500en_HK
dc.identifier.scopusauthoridShi, J=54882927400en_HK
dc.identifier.scopusauthoridWen, W=54883534700en_HK
dc.identifier.scopusauthoridLee, DH=54414374400en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK
dc.identifier.citeulike9835964-

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