Regulating axonal responses to injury: The intersection between signaling pathways involved in axon myelination and the inhibition of axon regeneration

Sudheendra N R Rao, Damien D Pearse

Research output: Contribution to journalReview article

17 Scopus citations

Abstract

Following spinal cord injury (SCI), a multitude of intrinsic and extrinsic factors adversely affect the gene programs that govern the expression of regeneration-associated genes (RAGs) and the production of a diversity of extracellular matrix molecules (ECM). Insufficient RAG expression in the injured neuron and the presence of inhibitory ECM at the lesion, leads to structural alterations in the axon that perturb the growth machinery, or form an extraneous barrier to axonal regeneration, respectively. Here, the role of myelin, both intact and debris, in antagonizing axon regeneration has been the focus of numerous investigations. These studies have employed antagonizing antibodies and knockout animals to examine how the growth cone of the re-growing axon responds to the presence of myelin and myelin-associated inhibitors (MAIs) within the lesion environment and caudal spinal cord. However, less attention has been placed on how the myelination of the axon after SCI, whether by endogenous glia or exogenously implanted glia, may alter axon regeneration. Here, we examine the intersection between intracellular signaling pathways in neurons and glia that are involved in axon myelination and axon growth, to provide greater insight into how interrogating this complex network of molecular interactions may lead to new therapeutics targeting SCI.

Original languageEnglish (US)
Article number33
JournalFrontiers in Molecular Neuroscience
Volume9
Issue numberJUNE
DOIs
StatePublished - Jun 8 2016

    Fingerprint

Keywords

  • Adaptive myelination
  • Axon regeneration
  • Myelination
  • Oligodendrocytes
  • Radial growth
  • Schwann cell
  • Signaling pathways
  • Spinal cord injuries

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Molecular Biology

Cite this