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Oligodendrocyte Regeneration and CNS Remyelination Require TACE/ADAM17.

Javier Palazuelos1, Michael Klingener2, Elaine W Raines3

  • 1Department of Pharmacological Sciences, Centers for Molecular Medicine, Stony Brook University, SUNY, Stony Brook, New York 11794, Adan.Aguirre@StonyBrook.edu Javier.PalazuelosDiego@StonyBrook.edu.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|September 5, 2015
PubMed
Summary

Tumor necrosis factor-alpha-converting enzyme (TACE) is crucial for oligodendrocyte regeneration and central nervous system (CNS) remyelination after demyelination. TACE supports oligodendrocyte survival and expansion, promoting myelin repair in demyelinating disorders.

Keywords:
ADAM17EGFRTACEoligodendrocyte precursorremyelination

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Area of Science:

  • Neuroscience
  • Regenerative Medicine
  • Molecular Biology

Background:

  • Oligodendrocyte (OL) regeneration is a key target for treating demyelinating disorders.
  • The role of TACE/ADAM17 in OL regeneration after demyelination was previously unknown.
  • TACE/ADAM17 regulates oligodendrogenesis during postnatal myelination.

Purpose of the Study:

  • To investigate the role of TACE/ADAM17 in oligodendrocyte regeneration and CNS remyelination following demyelination.
  • To determine if TACE is critical for EGFR activation in OLs after demyelination.
  • To explore therapeutic strategies for demyelinating disorders by targeting OL regeneration.

Main Methods:

  • Used genetic mouse models with selective gain- or loss-of-function of TACE or EGFR in OL lineage cells.
  • Assessed OL lineage cell expansion, survival, and CNS remyelination.
  • Investigated EGFR activation in OLs following demyelination.

Main Results:

  • TACE is critical for EGFR activation in OLs post-demyelination, supporting OL regeneration and CNS remyelination.
  • TACE deficiency in OL progenitor cells delays remyelination by impairing OL lineage cell expansion and survival.
  • EGFR overexpression in TACE-deficient OLs restores OL development and CNS remyelination.

Conclusions:

  • TACE plays an essential role in supporting OL regeneration and CNS remyelination.
  • Targeting TACE may offer new therapeutic strategies for promoting myelin repair in demyelinating disorders.
  • Understanding the TACE-EGFR pathway is vital for advancing regenerative medicine in demyelinating diseases.