Article: LINGO-1 antagonist promotes spinal cord remyelination and axonal integrity in MOG-induced experimental autoimmune encephalomyelitis

File Download Links for fulltext
(May Require Subscription)
Supplementary

  • Basic View
  • Metadata View
  • XML View
TitleLINGO-1 antagonist promotes spinal cord remyelination and axonal integrity in MOG-induced experimental autoimmune encephalomyelitis
AuthorsMi, S
Hu, B
Hahm, K
Luo, Y
Hui, ESK
Yuan, Q
Wong, WM
Wang, L
Su, H
Chu, TH
Guo, J
Zhang, W
So, KF2
Pepinsky, B
Shao, Z
Graff, C
Garber, E
Jung, V
Wu, EX2
Wu, W1 2
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
2011 Impact Factor: 22.462
2011 SCImago Journal Rankings: 4.452
DOIhttp://dx.doi.org/10.1038/nm1664
ReferencesReferences in Scopus
DC Field
Value
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.epage1233
dc.identifier.hkuros137876
dc.identifier.hkuros141487
dc.identifier.isiWOS:000249980200039
dc.identifier.issn1078-8956
2011 Impact Factor: 22.462
2011 SCImago Journal Rankings: 4.452
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
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