Schwann cell proliferation during Wallerian degeneration is not necessary for regeneration and remyelination of the peripheral nerves: Axon-dependent removal of newly generated Schwann cells by apoptosis

David P. Yang, Dan P. Zhang, Kimberley S. Mak, Daniel E. Bonder, Scott L. Pomeroy, Haesun A. Kim

Research output: Contribution to journalArticle

56 Scopus citations

Abstract

Peripheral nerve injury is followed by a wave of Schwann cell proliferation in the distal nerve stumps. To resolve the role of Schwann cell proliferation during functional recovery of the injured nerves, we used a mouse model in which injury-induced Schwann cell mitotic response is ablated via targeted disruption of cyclin D1. In the absence of distal Schwann cell proliferation, axonal regeneration and myelination occur normally in the mutant mice and functional recovery of injured nerves is achieved. This is enabled by pre-existing Schwann cells in the distal stump that persist but do not divide. On the other hand, in the wild type littermates, newly generated Schwann cells of injured nerves are culled by apoptosis. As a result, distal Schwann cell numbers in wild type and cyclin D1 null mice converge to equivalence in regenerated nerves. Therefore, distal Schwann cell proliferation is not required for functional recovery of injured nerves.

Original languageEnglish (US)
Pages (from-to)80-88
Number of pages9
JournalMolecular and Cellular Neuroscience
Volume38
Issue number1
DOIs
StatePublished - May 1 2008

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cellular and Molecular Neuroscience
  • Cell Biology

Keywords

  • Apoptosis
  • Cyclin D1
  • Functional recovery
  • Proliferation
  • Schwann cell
  • Wallerian degeneration

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