Show simple item record

dc.contributor.authorMoreau-Fauvarque, C
dc.contributor.authorKumanogoh, A
dc.contributor.authorCamand, E
dc.contributor.authorJaillard, C
dc.contributor.authorBarbin, G
dc.contributor.authorBoquet, I
dc.contributor.authorLove, C
dc.contributor.authorJones, EY
dc.contributor.authorKikutani, H
dc.contributor.authorLubetzki, C
dc.contributor.authorDusart, I
dc.contributor.authorChedotal, A
dc.date.accessioned2017-05-03T11:37:23Z
dc.date.available2017-05-03T11:37:23Z
dc.date.issued2003
dc.date.modified2009-09-03T07:17:04Z
dc.identifier.issn0270-6474
dc.identifier.urihttp://hdl.handle.net/10072/16924
dc.description.abstractSemaphorins are a family of secreted and membrane-bound proteins, known to regulate axonal pathfinding. Sema4D, also called CD100, was first isolated in the immune system where it is involved in B and T cell activation. We found that in the mouse, Sema4D is expressed in cells throughout the CNS white matter, with a peak during the myelination period. Double-labeling experiments with different markers of oligodendrocyte lineage such as olig1, olig2, platelet-derived growth factor receptor alpha, and proteolipid protein showed that Sema4D was expressed selectively by oligodendrocytes and myelin. The presence of Sema4D in myelin was confirmed using Western blot. Sema4D expression in myelinating oligodendrocytes was further observed using neuron-oligodendrocyte cocultures. Moreover, using stripe assay, we found that Sema4D is strongly inhibitory for postnatal sensory and cerebellar granule cell axons. This prompted us to examine whether Sema4D expression is modified after CNS injury. At 8 d after spinal cord lesions, Sema4D expression was strongly upregulated in oligodendrocytes at the periphery of the lesion. Sema4D-positive cells were not colabeled with the astrocyte marker GFAP, with the microglial and macrophagic marker isolectin B4, or with NG2, a marker of oligodendrocyte precursors. This upregulation was transient because from 1 month after the lesion, Sema4D expression was back to its normal level. These results indicate that Sema4D is a novel inhibitory factor for axonal regeneration expressed in myelin.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.format.extent1117867 bytes
dc.format.extent70629 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.languageEnglish
dc.language.isoen_AU
dc.publisherSociety for Neuroscience
dc.publisher.placeUnited States
dc.publisher.urihttp://www.jneurosci.org/content/23/27/9229
dc.relation.ispartofpagefrom9229
dc.relation.ispartofpageto9239
dc.relation.ispartofissue27
dc.relation.ispartofjournalJournal of Neuroscience
dc.relation.ispartofvolume23
dc.subject.fieldofresearchMedical and Health Sciences
dc.subject.fieldofresearchPsychology and Cognitive Sciences
dc.subject.fieldofresearchcode11
dc.subject.fieldofresearchcode17
dc.titleThe transmembrane semaphorin Sema4D/CD100, an inhibitor of axonal growth, is expressed on oligodendrocytes and upregulated after CNS lesion
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.rights.copyright© 2003 Society for Neuroscience. Reproduced in accordance with the copyright policy of the publisher. Please refer to the journal website for access to the definitive, published version.
gro.date.issued2003
gro.hasfulltextFull Text
gro.griffith.authorLove, Christopher A.


Files in this item

This item appears in the following Collection(s)

  • Journal articles
    Contains articles published by Griffith authors in scholarly journals.

Show simple item record