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Article: LINGO-1 negatively regulates TrkB phosphorylation after ocular hypertension

TitleLINGO-1 negatively regulates TrkB phosphorylation after ocular hypertension
Authors
Fu, QLHu, BLi, XShao, ZShi, JBWu, WSo, KFMi, S
KeywordsBrain-derived neurotrophic factor
Glaucoma
Intraocular pressure
Neuronal survival
Retinal ganglion cell
Issue Date2010
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/EJN
Citation
European Journal Of Neuroscience, 2010, v. 31 n. 6, p. 1091-1097 How to Cite?
DOI: http://dx.doi.org/10.1111/j.1460-9568.2010.07127.x
AbstractThe antagonism of LINGO-1, a CNS-specific negative regulator of neuronal survival, was shown to promote short-term survival of retinal ganglion cell (RGC) in an ocular hypertension model. LINGO-1 antagonists, combined with brain-derived neurotrophic factor (BDNF), can increase the length of neuron survival through an unclear molecular mechanism. To determine the relationship between LINGO-1 and BDNF/TrkB receptor in neuronal protection, we show here that LINGO-1 forms a receptor complex with TrkB and negatively regulates its activation in the retina after ocular hypertension injury. LINGO-1 antagonist antibody 1A7 or soluble LINGO-1 (LINGO-1-Fc) treatment upregulates phospho-TrkB phosphorylation and leads to RGC survival after high intraocular pressure injury. This neuronal protective effect was blocked by anti-BDNF antibody. LINGO-1 antagonism therefore promotes RGC survival by regulating the BDNF and TrkB signaling pathway after ocular hypertension. © Federation of European Neuroscience Societies and Blackwell Publishing Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/149736
ISSN
0953-816X
2021 Impact Factor: 3.698
2020 SCImago Journal Rankings: 1.346
ISI Accession Number ID
WOS:000275674400011
Funding AgencyGrant Number
The University of Hong Kong Foundation for Educational Development and Research Limited
NSFC30801272
RFDP200805581160
Natural Science Foundation of Guangdong Province of China8451008901000852
Training Foundation for the Youth Scholars of Sun Yat-Sen University2009009
2009026
Science and Technology Foundation of Guangdong Province of China2006B36004010
2008B030301090
Chinese Academy of Sciences
Funding Information:

This study was supported by funding from the Jessie Ho Professorship in Neuroscience (The University of Hong Kong Foundation for Educational Development and Research Limited, and donation from Mr George Ho), and donations from Ms Tung Shai Yun and Ms Annie Tsao Wen Wei. This research is also supported by grants from the NSFC (30801272), RFDP (200805581160), Natural Science Foundation of Guangdong Province of China (8451008901000852), Training Foundation for the Youth Scholars of Sun Yat-Sen University (2009009, 2009026) and The Science and Technology Foundation of Guangdong Province of China (2006B36004010, 2008B030301090). Bai Ren Ji Hua provided a grant to B.H. (Chinese Academy of Sciences).

References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorFu, QLen_US
dc.contributor.authorHu, Ben_US
dc.contributor.authorLi, Xen_US
dc.contributor.authorShao, Zen_US
dc.contributor.authorShi, JBen_US
dc.contributor.authorWu, Wen_US
dc.contributor.authorSo, KFen_US
dc.contributor.authorMi, Sen_US
dc.date.accessioned2012-06-26T05:57:49Z-
dc.date.available2012-06-26T05:57:49Z-
dc.date.issued2010en_US
dc.identifier.citationEuropean Journal Of Neuroscience, 2010, v. 31 n. 6, p. 1091-1097en_US
dc.identifier.issn0953-816Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/149736-
dc.description.abstractThe antagonism of LINGO-1, a CNS-specific negative regulator of neuronal survival, was shown to promote short-term survival of retinal ganglion cell (RGC) in an ocular hypertension model. LINGO-1 antagonists, combined with brain-derived neurotrophic factor (BDNF), can increase the length of neuron survival through an unclear molecular mechanism. To determine the relationship between LINGO-1 and BDNF/TrkB receptor in neuronal protection, we show here that LINGO-1 forms a receptor complex with TrkB and negatively regulates its activation in the retina after ocular hypertension injury. LINGO-1 antagonist antibody 1A7 or soluble LINGO-1 (LINGO-1-Fc) treatment upregulates phospho-TrkB phosphorylation and leads to RGC survival after high intraocular pressure injury. This neuronal protective effect was blocked by anti-BDNF antibody. LINGO-1 antagonism therefore promotes RGC survival by regulating the BDNF and TrkB signaling pathway after ocular hypertension. © Federation of European Neuroscience Societies and Blackwell Publishing Ltd.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/EJNen_US
dc.relation.ispartofEuropean Journal of Neuroscienceen_US
dc.subjectBrain-derived neurotrophic factor-
dc.subjectGlaucoma-
dc.subjectIntraocular pressure-
dc.subjectNeuronal survival-
dc.subjectRetinal ganglion cell-
dc.subject.meshAnimalsen_US
dc.subject.meshAntibodies - Pharmacology - Therapeutic Useen_US
dc.subject.meshBrain-Derived Neurotrophic Factor - Immunology - Metabolismen_US
dc.subject.meshCell Line, Transformeden_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expression Regulation - Drug Effects - Physiologyen_US
dc.subject.meshImmunoprecipitationen_US
dc.subject.meshIntraocular Pressure - Physiologyen_US
dc.subject.meshMembrane Proteins - Genetics - Immunology - Metabolismen_US
dc.subject.meshNerve Tissue Proteins - Genetics - Immunology - Metabolismen_US
dc.subject.meshOcular Hypertension - Drug Therapy - Metabolism - Pathologyen_US
dc.subject.meshPhosphorylation - Drug Effects - Physiologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptor, Trkb - Metabolismen_US
dc.subject.meshRetina - Pathologyen_US
dc.subject.meshRetinal Ganglion Cells - Metabolism - Pathologyen_US
dc.subject.meshTime Factorsen_US
dc.titleLINGO-1 negatively regulates TrkB phosphorylation after ocular hypertensionen_US
dc.typeArticleen_US
dc.identifier.emailWu, W:wtwu@hkucc.hku.hken_US
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_US
dc.identifier.authorityWu, W=rp00419en_US
dc.identifier.authoritySo, KF=rp00329en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1460-9568.2010.07127.xen_US
dc.identifier.pmid20377621-
dc.identifier.scopuseid_2-s2.0-77949543242en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77949543242&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume31en_US
dc.identifier.issue6en_US
dc.identifier.spage1091en_US
dc.identifier.epage1097en_US
dc.identifier.isiWOS:000275674400011-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridFu, QL=23388762000en_US
dc.identifier.scopusauthoridHu, B=35733928400en_US
dc.identifier.scopusauthoridLi, X=36064257300en_US
dc.identifier.scopusauthoridShao, Z=7202244441en_US
dc.identifier.scopusauthoridShi, JB=26025986700en_US
dc.identifier.scopusauthoridWu, W=7407081122en_US
dc.identifier.scopusauthoridSo, KF=34668391300en_US
dc.identifier.scopusauthoridMi, S=7004825561en_US
dc.identifier.citeulike6885051-
dc.identifier.issnl0953-816X-

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