4.6 Article

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

Journal

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 514, Issue 4, Pages 1037-1039

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2019.05.060

Keywords

Neurodegeneration; Phosphorylation; Optic nerve; Genetic; Mouse

Funding

  1. Ministry of Education, Culture, Sports, Science and Technology [26430043, 17082006]
  2. Core Research for Evolutional Science and Technology of Japan Science and Technology Agency
  3. Creation of Innovation Centers for Advanced Interdisciplinary Research Areas Program in the Project for Developing Innovation System from the MEXT [42890001]

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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 3 beta (GSK3 beta), and it is involved in Wallerian degeneration after optic nerve injury. We previously developed a CRMP2 knock-in (CRMP2 RI) mouse line, in which CRMP2 phosphorylation by GSK3 beta is inhibited; however, Wallerian degeneration in CRMP2 RI mice has not yet been examined. In this study, we examined whether Wallerian degeneration of the optic nerve is suppressed in CRMP2 RI 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. (C) 2019 Elsevier Inc. All rights reserved.

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