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Piaton, G.* ; Aigrot, M.S.* ; Williams, A.* ; Moyon, S.* ; Tepavcevic, V.* ; Moutkine, I.* ; Gras, J.* ; Matho, K.S.* ; Schmitt, A.* ; Soellner, H. ; Huber, A.B. ; Ravassard, P.* ; Lubetzki, C.*

Class 3 semaphorins influence oligodendrocyte precursor recruitment and remyelination in adult central nervous system.

Brain 134, 1156-1167 (2011)

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Open Access Green as soon as Postprint is submitted to ZB.

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Oligodendrocyte precursor cells, which persist in the adult central nervous system, are the main source of central nervous system remyelinating cells. In multiple sclerosis, some demyelinated plaques exhibit an oligodendroglial depopulation, raising the hypothesis of impaired oligodendrocyte precursor cell recruitment. Developmental studies identified semaphorins 3A and 3F as repulsive and attractive guidance cues for oligodendrocyte precursor cells, respectively. We previously reported their increased expression in experimental demyelination and in multiple sclerosis. Here, we show that adult oligodendrocyte precursor cells, like their embryonic counterparts, express class 3 semaphorin receptors, neuropilins and plexins and that neuropilin expression increases after demyelination. Using gain and loss of function experiments in an adult murine demyelination model, we demonstrate that semaphorin 3A impairs oligodendrocyte precursor cell recruitment to the demyelinated area. In contrast, semaphorin 3F overexpression accelerates not only oligodendrocyte precursor cell recruitment, but also remyelination rate. These data open new avenues to understand remyelination failure and promote repair in multiple sclerosis.

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Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords semaphorin; oligodendrocyte precursor cell; recruitment; remyelination; gain and loss of function

ISSN (print) / ISBN 0006-8950

e-ISSN 1460-2156

Journal Brain: A Journal of Neurology

Quellenangaben Volume: 134, Issue: 4, Pages: 1156-1167

Publisher Oxford University Press

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) Institute of Developmental Genetics (IDG)