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Article: LINGO-1 antagonist promotes spinal cord remyelination and axonal integrity in MOG-induced experimental autoimmune encephalomyelitis
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TitleLINGO-1 antagonist promotes spinal cord remyelination and axonal integrity in MOG-induced experimental autoimmune encephalomyelitis
 
AuthorsMi, S3
Hu, B2 4
Hahm, K3
Luo, Y3
Hui, ESK2
Yuan, Q2
Wong, WM2
Wang, L2
Su, H2
Chu, TH2
Guo, J2
Zhang, W2
So, KF2
Pepinsky, B3
Shao, Z3
Graff, C3
Garber, E3
Jung, V3
Wu, EX2
Wu, W2 1
 
Issue Date2007
 
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/nm
 
CitationNature Medicine, 2007, v. 13 n. 10, p. 1228-1233 [How to Cite?]
DOI: http://dx.doi.org/10.1038/nm1664
 
AbstractDemyelinating diseases, such as multiple sclerosis, are characterized by the loss of the myelin sheath around neurons, owing to inflammation and gliosis in the central nervous system (CNS). Current treatments therefore target anti-inflammatory mechanisms to impede or slow disease progression. The identification of a means to enhance axon myelination would present new therapeutic approaches to inhibit and possibly reverse disease progression. Previously, LRR and Ig domain-containing, Nogo receptor-interacting protein (LINGO-1) has been identified as an in vitro and in vivo negative regulator of oligodendrocyte differentiation and myelination. Here we show that loss of LINGO-1 function by Lingo1 gene knockout or by treatment with an antibody antagonist of LINGO-1 function leads to functional recovery from experimental autoimmune encephalomyelitis. This is reflected biologically by improved axonal integrity, as confirmed by magnetic resonance diffusion tensor imaging, and by newly formed myelin sheaths, as determined by electron microscopy. Antagonism of LINGO-1 or its pathway is therefore a promising approach for the treatment of demyelinating diseases of the CNS. © 2007 Nature Publishing Group.
 
ISSN1078-8956
2013 Impact Factor: 28.054
2013 SCImago Journal Rankings: 10.988
 
DOIhttp://dx.doi.org/10.1038/nm1664
 
ISI Accession Number IDWOS:000249980200039
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorMi, S
 
dc.contributor.authorHu, B
 
dc.contributor.authorHahm, K
 
dc.contributor.authorLuo, Y
 
dc.contributor.authorHui, ESK
 
dc.contributor.authorYuan, Q
 
dc.contributor.authorWong, WM
 
dc.contributor.authorWang, L
 
dc.contributor.authorSu, H
 
dc.contributor.authorChu, TH
 
dc.contributor.authorGuo, J
 
dc.contributor.authorZhang, W
 
dc.contributor.authorSo, KF
 
dc.contributor.authorPepinsky, B
 
dc.contributor.authorShao, Z
 
dc.contributor.authorGraff, C
 
dc.contributor.authorGarber, E
 
dc.contributor.authorJung, V
 
dc.contributor.authorWu, EX
 
dc.contributor.authorWu, W
 
dc.date.accessioned2010-09-06T05:57:26Z
 
dc.date.available2010-09-06T05:57:26Z
 
dc.date.issued2007
 
dc.description.abstractDemyelinating diseases, such as multiple sclerosis, are characterized by the loss of the myelin sheath around neurons, owing to inflammation and gliosis in the central nervous system (CNS). Current treatments therefore target anti-inflammatory mechanisms to impede or slow disease progression. The identification of a means to enhance axon myelination would present new therapeutic approaches to inhibit and possibly reverse disease progression. Previously, LRR and Ig domain-containing, Nogo receptor-interacting protein (LINGO-1) has been identified as an in vitro and in vivo negative regulator of oligodendrocyte differentiation and myelination. Here we show that loss of LINGO-1 function by Lingo1 gene knockout or by treatment with an antibody antagonist of LINGO-1 function leads to functional recovery from experimental autoimmune encephalomyelitis. This is reflected biologically by improved axonal integrity, as confirmed by magnetic resonance diffusion tensor imaging, and by newly formed myelin sheaths, as determined by electron microscopy. Antagonism of LINGO-1 or its pathway is therefore a promising approach for the treatment of demyelinating diseases of the CNS. © 2007 Nature Publishing Group.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationNature Medicine, 2007, v. 13 n. 10, p. 1228-1233 [How to Cite?]
DOI: http://dx.doi.org/10.1038/nm1664
 
dc.identifier.citeulike1794754
 
dc.identifier.doihttp://dx.doi.org/10.1038/nm1664
 
dc.identifier.eissn1546-170X
 
dc.identifier.epage1233
 
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dc.identifier.isiWOS:000249980200039
 
dc.identifier.issn1078-8956
2013 Impact Factor: 28.054
2013 SCImago Journal Rankings: 10.988
 
dc.identifier.issue10
 
dc.identifier.openurl
 
dc.identifier.pmid17906634
 
dc.identifier.scopuseid_2-s2.0-34948888764
 
dc.identifier.spage1228
 
dc.identifier.urihttp://hdl.handle.net/10722/67696
 
dc.identifier.volume13
 
dc.languageeng
 
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/nm
 
dc.publisher.placeUnited States
 
dc.relation.ispartofNature Medicine
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAnimals
 
dc.subject.meshAxons - physiology - radiography - ultrastructure
 
dc.subject.meshEncephalomyelitis, Autoimmune, Experimental - chemically induced - pathology
 
dc.subject.meshInjections, Spinal
 
dc.subject.meshMembrane Proteins - administration & dosage - antagonists & inhibitors - physiology
 
dc.subject.meshMice
 
dc.subject.meshMice, Knockout
 
dc.subject.meshMyelin Proteins
 
dc.subject.meshMyelin Sheath - physiology - ultrastructure
 
dc.subject.meshMyelin-Associated Glycoprotein - immunology - pharmacology
 
dc.subject.meshNerve Tissue Proteins - administration & dosage - antagonists & inhibitors - physiology
 
dc.subject.meshRats
 
dc.subject.meshSpinal Cord Injuries - pathology - physiopathology - therapy
 
dc.subject.meshTomography, X-Ray Computed
 
dc.titleLINGO-1 antagonist promotes spinal cord remyelination and axonal integrity in MOG-induced experimental autoimmune encephalomyelitis
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. The University of Hong Kong
  3. Biogen IDEC
  4. University of Science and Technology of China