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

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TitleLINGO-1 negatively regulates TrkB phosphorylation after ocular hypertension
AuthorsFu, QL1 4
Hu, B1 3
Li, X4
Shao, Z2
Shi, JB4
Wu, W1 5
So, KF1 5
Mi, S2
Issue Date2010
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/EJN
CitationEuropean 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.
ISSN0953-816X
2011 Impact Factor: 3.631
2011 SCImago Journal Rankings: 0.359
DOIhttp://dx.doi.org/10.1111/j.1460-9568.2010.07127.x
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorFu, QL
dc.contributor.authorHu, B
dc.contributor.authorLi, X
dc.contributor.authorShao, Z
dc.contributor.authorShi, JB
dc.contributor.authorWu, W
dc.contributor.authorSo, KF
dc.contributor.authorMi, S
dc.date.accessioned2012-06-26T05:57:49Z
dc.date.available2012-06-26T05:57:49Z
dc.date.issued2010
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.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationEuropean 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
dc.identifier.citeulike6885051
dc.identifier.doihttp://dx.doi.org/10.1111/j.1460-9568.2010.07127.x
dc.identifier.epage1097
dc.identifier.isiWOS: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).

dc.identifier.issn0953-816X
2011 Impact Factor: 3.631
2011 SCImago Journal Rankings: 0.359
dc.identifier.issue6
dc.identifier.pmid20377621
dc.identifier.scopuseid_2-s2.0-77949543242
dc.identifier.spage1091
dc.identifier.urihttp://hdl.handle.net/10722/149736
dc.identifier.volume31
dc.languageeng
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/EJN
dc.publisher.placeUnited Kingdom
dc.relation.ispartofEuropean Journal of Neuroscience
dc.relation.referencesReferences in Scopus
dc.subject.meshAnimals
dc.subject.meshAntibodies - Pharmacology - Therapeutic Use
dc.subject.meshBrain-Derived Neurotrophic Factor - Immunology - Metabolism
dc.subject.meshCell Line, Transformed
dc.subject.meshDisease Models, Animal
dc.subject.meshFemale
dc.subject.meshGene Expression Regulation - Drug Effects - Physiology
dc.subject.meshImmunoprecipitation
dc.subject.meshIntraocular Pressure - Physiology
dc.subject.meshMembrane Proteins - Genetics - Immunology - Metabolism
dc.subject.meshNerve Tissue Proteins - Genetics - Immunology - Metabolism
dc.subject.meshOcular Hypertension - Drug Therapy - Metabolism - Pathology
dc.subject.meshPhosphorylation - Drug Effects - Physiology
dc.subject.meshRats
dc.subject.meshRats, Sprague-Dawley
dc.subject.meshReceptor, Trkb - Metabolism
dc.subject.meshRetina - Pathology
dc.subject.meshRetinal Ganglion Cells - Metabolism - Pathology
dc.subject.meshTime Factors
dc.titleLINGO-1 negatively regulates TrkB phosphorylation after ocular hypertension
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. Biogen IDEC
  3. University of Science and Technology of China
  4. Sun Yat-Sen University
  5. Jinan University