File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

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

TitleLINGO-1 antagonist promotes spinal cord remyelination and axonal integrity in MOG-induced experimental autoimmune encephalomyelitis
Authors
Issue Date2007
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/nm
Citation
Nature Medicine, 2007, v. 13 n. 10, p. 1228-1233 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/67696
ISSN
2015 Impact Factor: 30.357
2015 SCImago Journal Rankings: 13.959
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMi, Sen_HK
dc.contributor.authorHu, Ben_HK
dc.contributor.authorHahm, Ken_HK
dc.contributor.authorLuo, Yen_HK
dc.contributor.authorHui, ESKen_HK
dc.contributor.authorYuan, Qen_HK
dc.contributor.authorWong, WMen_HK
dc.contributor.authorWang, Len_HK
dc.contributor.authorSu, Hen_HK
dc.contributor.authorChu, THen_HK
dc.contributor.authorGuo, Jen_HK
dc.contributor.authorZhang, Wen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorPepinsky, Ben_HK
dc.contributor.authorShao, Zen_HK
dc.contributor.authorGraff, Cen_HK
dc.contributor.authorGarber, Een_HK
dc.contributor.authorJung, Ven_HK
dc.contributor.authorWu, EXen_HK
dc.contributor.authorWu, Wen_HK
dc.date.accessioned2010-09-06T05:57:26Z-
dc.date.available2010-09-06T05:57:26Z-
dc.date.issued2007en_HK
dc.identifier.citationNature Medicine, 2007, v. 13 n. 10, p. 1228-1233en_HK
dc.identifier.issn1078-8956en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67696-
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.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/nmen_HK
dc.relation.ispartofNature Medicineen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAxons - physiology - radiography - ultrastructureen_HK
dc.subject.meshEncephalomyelitis, Autoimmune, Experimental - chemically induced - pathologyen_HK
dc.subject.meshInjections, Spinalen_HK
dc.subject.meshMembrane Proteins - administration & dosage - antagonists & inhibitors - physiologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Knockouten_HK
dc.subject.meshMyelin Proteinsen_HK
dc.subject.meshMyelin Sheath - physiology - ultrastructureen_HK
dc.subject.meshMyelin-Associated Glycoprotein - immunology - pharmacologyen_HK
dc.subject.meshNerve Tissue Proteins - administration & dosage - antagonists & inhibitors - physiologyen_HK
dc.subject.meshRatsen_HK
dc.subject.meshSpinal Cord Injuries - pathology - physiopathology - therapyen_HK
dc.subject.meshTomography, X-Ray Computeden_HK
dc.titleLINGO-1 antagonist promotes spinal cord remyelination and axonal integrity in MOG-induced experimental autoimmune encephalomyelitisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1078-8956&volume=13&issue=10&spage=1228&epage=1233&date=2007&atitle=LINGO-1+antagonist+promotes+spinal+cord+remyelination+and+axonal+integrity+in+MOG-induced+experimental+autoimmune+encephalomyelitisen_HK
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_HK
dc.identifier.emailWu, EX:ewu1@hkucc.hku.hken_HK
dc.identifier.emailWu, W:wtwu@hkucc.hku.hken_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityWu, EX=rp00193en_HK
dc.identifier.authorityWu, W=rp00419en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/nm1664en_HK
dc.identifier.pmid17906634-
dc.identifier.scopuseid_2-s2.0-34948888764en_HK
dc.identifier.hkuros137876en_HK
dc.identifier.hkuros141487-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34948888764&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume13en_HK
dc.identifier.issue10en_HK
dc.identifier.spage1228en_HK
dc.identifier.epage1233en_HK
dc.identifier.eissn1546-170X-
dc.identifier.isiWOS:000249980200039-
dc.publisher.placeUnited Statesen_HK
dc.identifier.f10001092191-
dc.identifier.scopusauthoridMi, S=7004825561en_HK
dc.identifier.scopusauthoridHu, B=35733928400en_HK
dc.identifier.scopusauthoridHahm, K=7101829744en_HK
dc.identifier.scopusauthoridLuo, Y=55187941300en_HK
dc.identifier.scopusauthoridKam Hui, ES=22234110800en_HK
dc.identifier.scopusauthoridYuan, Q=7202814773en_HK
dc.identifier.scopusauthoridWong, WM=7403972413en_HK
dc.identifier.scopusauthoridWang, L=7409182141en_HK
dc.identifier.scopusauthoridSu, H=16317750200en_HK
dc.identifier.scopusauthoridChu, TH=14023966500en_HK
dc.identifier.scopusauthoridGuo, J=7404488603en_HK
dc.identifier.scopusauthoridZhang, W=9044147100en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK
dc.identifier.scopusauthoridPepinsky, B=6603558137en_HK
dc.identifier.scopusauthoridShao, Z=7202244441en_HK
dc.identifier.scopusauthoridGraff, C=7006516493en_HK
dc.identifier.scopusauthoridGarber, E=35310012100en_HK
dc.identifier.scopusauthoridJung, V=7006727074en_HK
dc.identifier.scopusauthoridWu, EX=7202128034en_HK
dc.identifier.scopusauthoridWu, W=7407081122en_HK
dc.identifier.citeulike1794754-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats