PT  - JOURNAL ARTICLE
AU  - P. Assinck
AU  - G.J. Duncan
AU  - J.R. Plemel
AU  - M.J. Lee
AU  - J.S. Stratton
AU  - S.B. Manesh
AU  - J. Liu
AU  - L.M. Ramer
AU  - S.H. Kang
AU  - D.E. Bergles
AU  - J. Biernaskie
AU  - W. Tetzlaff
TI  - Myelinogenic plasticity of oligodendrocyte precursor cells following spinal cord contusion injury.
AID  - 10.1523/JNEUROSCI.2409-16.2017
DP  - 2017 Jul 31
TA  - The Journal of Neuroscience
PG  - 2409-16
4099  - http://www.jneurosci.org/content/early/2017/07/31/JNEUROSCI.2409-16.2017.short
4100  - http://www.jneurosci.org/content/early/2017/07/31/JNEUROSCI.2409-16.2017.full
AB  - Spontaneous remyelination occurs after spinal cord injury (SCI), but the extent of myelin repair and identity of the cells responsible remain incompletely understood and contentious. We assessed the cellular origin of new myelin by fate mapping PDGFRα+, Olig2+, and P0+ cells following contusion SCI in mice. Oligodendrocyte precursor cells (OPCs; PDGFRα+) produced oligodendrocytes responsible for de novo ensheathment of ∼30% of myelinated spinal axons at injury epicenter three months after SCI, demonstrating that these resident cells are a major contributor to oligodendrocyte regeneration. OPCs also produced the majority of myelinating Schwann cells in the injured spinal cord; invasion of peripheral myelinating (P0+) Schwann cells made only a limited contribution. These findings reveal that PDGFRα+ cells perform diverse roles in central nervous system (CNS) repair, as multipotential progenitors that generate both classes of myelinating cells. This endogenous repair might be exploited as a therapeutic target for CNS trauma and disease.Significance Statement: Spinal cord injury (SCI) leads to profound functional deficits, though substantial numbers of axons often survive. One possible explanation is loss of myelin, creating conduction block at the site of injury. SCI leads to oligodendrocyte death and demyelination, and clinical trials have tested glial transplants to promote myelin repair. However, the degree and duration of myelin loss, and the extent and mechanisms of endogenous repair, have been contentious issues. Here, we use genetic fate mapping to demonstrate that spontaneous myelin repair by endogenous oligodendrocyte precursors (OPCs) is much more robust than previously recognized. These findings are relevant to many types of CNS pathology, raising the possibility that CNS precursors could be manipulated to repair myelin in lieu of glial transplantation.