Genetic inhibition of CRMP2 phosphorylation delays Wallerian degeneration after optic nerve injury

Yuki Kinoshita, Syunsuke Kondo, Kazuya Takahashi, Jun Nagai, Shuji Wakatsuki, Toshiyuki Araki, Yoshio Goshima, Toshio Ohshima

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Axonal degeneration occurs in patients with various neurological diseases and traumatic nerve injuries, and Wallerian degeneration is a phenomenon in the prototypical axonal degradation that is observed after injury. Collapsin response mediator protein 2 (CRMP2)is phosphorylated by glycogen synthase kinase 3β (GSK3β), and it is involved in Wallerian degeneration after optic nerve injury. We previously developed a CRMP2 knock-in (CRMP2 KI)mouse line, in which CRMP2 phosphorylation by GSK3β is inhibited; however, Wallerian degeneration in CRMP2 KI mice has not yet been examined. In this study, we examined whether Wallerian degeneration of the optic nerve is suppressed in CRMP2 KI mice. Using one eye removal model, we compared Wallerian degeneration of the optic nerve based on histological and biochemical analyses. Our experimental results indicated that the genetic inhibition of CRMP2 phosphorylation delays Wallerian degeneration after optic nerve injury.

Original languageEnglish
Pages (from-to)1037-1039
Number of pages3
JournalBiochemical and Biophysical Research Communications
Volume514
Issue number4
DOIs
Publication statusPublished - 2019 Jul 5

Keywords

  • Genetic
  • Mouse
  • Neurodegeneration
  • Optic nerve
  • Phosphorylation

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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