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Cited by 498

Chronic stage multiple sclerosis lesions contain a relatively quiescent population of oligodendrocyte precursor cells

Wolswijk, Guus·1998·The Journal of Neuroscience
DOI 10.1523/jneurosci.18-02-00601.1998
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Abstract

In the past decade, considerable progress has been made in the understanding of the biology of rodent oligodendrocyte precursor cells and their role in the generation of oligodendrocytes in the developing and adult rodent CNS. Much less is known about human oligodendrocyte lineage cells and about the reasons for the failure of the regeneration of the oligodendrocyte population during chronic stages of multiple sclerosis (MS). In particular, the fate of the oligodendrocyte precursor population in MS has remained elusive. The present study examined the possibility that oligodendrocyte regeneration ultimately fails because of the local destruction of both oligodendrocytes and their precursor cells. Analysis of chronic stage MS tissue suggested that this is not the case, because all chronic MS lesions studied contained significant numbers of oligodendrocyte precursor cells, identified as process-bearing cells that bound the O4 antibody but not antibodies to GalC and GFAP. The oligodendrocyte precursor cells appeared, however, to be relatively quiescent, because none expressed the nuclear proliferation antigen recognized by the Ki-67 antibody, and because most lesions lacked myelinating oligodendrocytes in their centers. Thus, it appears that the regeneration of the oligodendrocyte population fails during chronic stages of MS because of the inability of oligodendrocyte precursor cells to proliferate and differentiate rather than because of the local destruction of all oligodendrocyte lineage cells. The identification of ways of stimulating the endogenous oligodendrocyte precursor population to expand and generate remyelinating cells may represent an alternative to transplantation of oligodendrocyte lineage cells to promote myelin repair in MS.

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Crossref · 10.1523/jneurosci.18-02-00601.1998

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  • In MS, remyelination is blocked at the differentiation/remyelination stage rather than during OPC recruitment.

    “In MS lesions, OPCs are recruited but fail to differentiate into myelinating OLs, suggesting that remyelination is blocked at the differentiation and remyelination stage rather than during OPC recruitment (Chang et al., 2002; Kuhlmann et al., 2008; Wolswijk, 1998).”

    From miR-219 Cooperates with miR-338 in Myelination and Promotes Myelin Repair in the CNS (2017) · cites this paper as Wolswijk, 1998

  • In MS lesions, OPCs are recruited but fail to differentiate into myelinating OLs.

    “In MS lesions, OPCs are recruited but fail to differentiate into myelinating OLs, suggesting that remyelination is blocked at the differentiation and remyelination stage rather than during OPC recruitment (Chang et al., 2002; Kuhlmann et al., 2008; Wolswijk, 1998).”

    From miR-219 Cooperates with miR-338 in Myelination and Promotes Myelin Repair in the CNS (2017) · cites this paper as Wolswijk, 1998

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Research works printed but not linked: 1

  1. Wolswijk G, Noble M (1995) In vitro studies of the development, main- tenance and regeneration of the oligodendrocyte-type-2 astrocyte (O- 2A) lineage in the adult central nervous system. In: Neuroglial cells (Kettenmann H, Ransom BR, eds), pp 149 -161. Oxford: Oxford UP.

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Authors
Wolswijk, G.
Venue
The Journal of Neuroscience
Publisher
Society for Neuroscience
Published
1998-01-15
Volume
18
Issue
2
Pages
601-609
ISSN
  • 0270-6474
  • 1529-2401
DOI
10.1523/jneurosci.18-02-00601.1998
Cited by
498
References
2
Language
en
Licence
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 181 d)

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