The fate and function of oligodendrocyte progenitor cells after traumatic spinal cord injury. Issue 2 (21st August 2019)

• Record Type: Journal Article
• Authors: Duncan, Greg J.; Manesh, Sohrab B.; Hilton, Brett J.; Assinck, Peggy; Plemel, Jason R.; Tetzlaff, Wolfram
• Is Part Of: Glia. Volume 68:Issue 2(2020)
• Page Start: 227
• Page End: 245
• Publication Date: 2019-08-21
• Subjects: oligodendrocyte -- oligodendrocyte progenitor cell -- remyelination -- Schwann cell -- spinal cord injury; Neuroglia -- Periodicals; Neurology -- Periodicals; 611.0188
• DOI: 10.1002/glia.23706
• Languages: English
• ISSNs: 0894-1491

Abstract

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. Main points: Oligodendrocyte progenitor cells (OPCs) differentiate into oligodendrocytes, Schwann cells and astrocytes after spinal cord injury (SCI). OPC‐derived oligodendrocytes and Schwann cells remyelinate nearly all intact demyelinated axons in rodent models of SCI. OPCs modulate neuroinflammation and contribute to the glial scar, where they likely restrict axon growth.