Myelin status and oligodendrocyte lineage cells over time after spinal cord injury: What do we know and what still needs to be unwrapped?. Issue 11 (24th August 2019)

• Record Type: Journal Article
• Authors: Pukos, Nicole; Goodus, Matthew T.; Sahinkaya, Fatma R.; McTigue, Dana M.
• Other Names: Fields R. Douglas guestEditor.; Richardson William D. guestEditor.
• Is Part Of: Glia. Volume 67:Issue 11(2019)
• Page Start: 2178
• Page End: 2202
• Publication Date: 2019-08-24
• Subjects: axon regeneration -- differentiation -- glutamate -- myelination -- NG2 cells -- proliferation; Neuroglia -- Periodicals; Neurology -- Periodicals; 611.0188
• DOI: 10.1002/glia.23702
• Languages: English
• ISSNs: 0894-1491

Abstract

Abstract: Spinal cord injury (SCI) affects over 17, 000 individuals in the United States per year, resulting in sudden motor, sensory and autonomic impairments below the level of injury. These deficits may be due at least in part to the loss of oligodendrocytes and demyelination of spared axons as it leads to slowed or blocked conduction through the lesion site. It has long been accepted that progenitor cells form new oligodendrocytes after SCI, resulting in the acute formation of new myelin on demyelinated axons. However, the chronicity of demyelination and the functional significance of remyelination remain contentious. Here we review work examining demyelination and remyelination after SCI as well as the current understanding of oligodendrocyte lineage cell responses to spinal trauma, including the surprisingly long‐lasting response of NG2+ oligodendrocyte progenitor cells (OPCs) to proliferate and differentiate into new myelinating oligodendrocytes for months after SCI. OPCs are highly sensitive to microenvironmental changes, and therefore respond to the ever‐changing post‐SCI milieu, including influx of blood, monocytes and neutrophils; activation of microglia and macrophages; changes in cytokines, chemokines and growth factors such as ciliary neurotrophic factor and fibroblast growth factor‐2; glutamate excitotoxicity; and axon degeneration and sprouting. We discuss how these changes relate to spontaneous oligodendrogenesis and remyelination, the evidence for and against demyelination being an important clinical problem and if remyelination contributes to motor recovery. Main points: Oligodendrocyte formation persists for months after spinal cord injury, resulting in the formation of new myelin on demyelinated axons, in spite of fluctuating intraspinal conditions over time. The chronicity and significance are discussed herein.