NG2 cell response in the CNP-EGFP mouse after contusive spinal cord injury

Glia. 2009 Feb;57(3):270-85. doi: 10.1002/glia.20755.

Abstract

NG2(+) cells in the adult CNS are a heterogeneous population. The extent to which the subpopulation of NG2(+) cells that function as oligodendrocyte progenitor cells (OPCs) respond to spinal cord injury (SCI) and recapitulate their normal developmental progression remains unclear. We used the CNP-EGFP mouse, in which oligodendrocyte lineage cells express EGFP, to study NG2(+) cells in the normal and injured spinal cord. In white matter of uninjured mice, bipolar EGFP(+)NG2(+) cells and multipolar EGFP(neg)NG2(+) cells were identified. After SCI, EGFP(+)NG2(+) cell proliferation in residual white matter peaked at 3 days post injury (DPI) rostral to the epicenter, while EGFP(neg)NG2(+) cell proliferation peaked at 7 DPI at the epicenter. The expression of transcription factors, Olig2, Sox10, and Sox17, and the basic electrophysiological membrane parameters and potassium current phenotype of the EGFP(+)NG2(+) population after injury were consistent with those of proliferative OPCs during development. EGFP(neg)NG2(+) cells did not express transcription factors involved in oligodendrogenesis. EGFP(+)CC1(+) oligodendrocytes at 6 weeks included cells that incorporated BrdU during the peak of EGFP(+)NG2(+) cell proliferation. EGFP(neg)CC1(+) oligodendrocytes were never observed. Treatment with glial growth factor 2 and fibroblast growth factor 2 enhanced oligodendrogenesis and increased the number of EGFP(neg)NG2(+) cells. Therefore, based on EGFP and transcription factor expression, spatiotemporal proliferation patterns, and response to growth factors, two populations of NG2(+) cells can be identified that react to SCI. The EGFP(+)NG2(+) cells undergo cellular and physiological changes in response to SCI that are similar to those that occur in early postnatal NG2(+) cells during developmental oligodendrogenesis.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Action Potentials / drug effects
  • Action Potentials / genetics
  • Adult Stem Cells / drug effects
  • Adult Stem Cells / physiology*
  • Animals
  • Basic Helix-Loop-Helix Transcription Factors / metabolism
  • Behavior, Animal
  • Bromodeoxyuridine / metabolism
  • Cell Proliferation / drug effects
  • Cyclic Nucleotide Phosphodiesterases, Type 3 / genetics
  • Disease Models, Animal
  • Fibroblast Growth Factor 2 / pharmacology
  • Gene Expression Regulation / genetics
  • Gene Expression Regulation / physiology
  • Green Fluorescent Proteins / genetics
  • HMGB Proteins / metabolism
  • Mice
  • Mice, Transgenic
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism
  • Nerve Tissue Proteins / pharmacology
  • Neuregulin-1
  • Oligodendrocyte Transcription Factor 2
  • Oligodendroglia / drug effects
  • Oligodendroglia / physiology*
  • Potassium Channels, Voltage-Gated / metabolism
  • SOXE Transcription Factors / metabolism
  • SOXF Transcription Factors / metabolism
  • Spinal Cord Injuries / drug therapy
  • Spinal Cord Injuries / pathology*
  • Spinal Cord Injuries / physiopathology*
  • Time Factors

Substances

  • Basic Helix-Loop-Helix Transcription Factors
  • HMGB Proteins
  • Nerve Tissue Proteins
  • Neuregulin-1
  • Nrg1 protein, mouse
  • Olig2 protein, mouse
  • Oligodendrocyte Transcription Factor 2
  • Potassium Channels, Voltage-Gated
  • SOXE Transcription Factors
  • SOXF Transcription Factors
  • Sox10 protein, mouse
  • Sox17 protein, mouse
  • enhanced green fluorescent protein
  • Fibroblast Growth Factor 2
  • Green Fluorescent Proteins
  • Cyclic Nucleotide Phosphodiesterases, Type 3
  • Bromodeoxyuridine