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Glia. 2019 Aug 21. doi: 10.1002/glia.23706. [Epub ahead of print]

The fate and function of oligodendrocyte progenitor cells after traumatic spinal cord injury.

Author information

1
Department of Neurology, Jungers Center for Neurosciences Research, Oregon Health and Science University, Portland, Oregon.
2
Graduate Program in Neuroscience, International Collaboration on Repair Discoveries (ICORD), University of British Columbia (UBC), Vancouver, British Columbia, Canada.
3
Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Bonn, Germany.
4
MRC Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.
5
Department of Medicine, Division of Neurology, Neuroscience and Mental Health Institute, University of Alberta, Calgary, Alberta, Canada.
6
Departments of Zoology and Surgery, University of British Columbia, Vancouver, British Columbia, Canada.

Abstract

Oligodendrocyte progenitor cells (OPCs) are the most proliferative and dispersed population of progenitor cells in the adult central nervous system, which allows these cells to rapidly respond to damage. Oligodendrocytes and myelin are lost after traumatic spinal cord injury (SCI), compromising efficient conduction and, potentially, the long-term health of axons. In response, OPCs proliferate and then differentiate into new oligodendrocytes and Schwann cells to remyelinate axons. This culminates in highly efficient remyelination following experimental SCI in which nearly all intact demyelinated axons are remyelinated in rodent models. However, myelin regeneration comprises only one role of OPCs following SCI. OPCs contribute to scar formation after SCI and restrict the regeneration of injured axons. Moreover, OPCs alter their gene expression following demyelination, express cytokines and perpetuate the immune response. Here, we review the functional contribution of myelin regeneration and other recently uncovered roles of OPCs and their progeny to repair following SCI.

KEYWORDS:

Schwann cell; oligodendrocyte; oligodendrocyte progenitor cell; remyelination; spinal cord injury

PMID:
31433109
DOI:
10.1002/glia.23706

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