| First Author | Kinoshita Y | Year | 2019 |
| Journal | Biochem Biophys Res Commun | Volume | 514 |
| Issue | 4 | Pages | 1037-1039 |
| PubMed ID | 31097218 | Mgi Jnum | J:291792 |
| Mgi Id | MGI:6443507 | Doi | 10.1016/j.bbrc.2019.05.060 |
| Citation | Kinoshita Y, et al. (2019) Genetic inhibition of CRMP2 phosphorylation delays Wallerian degeneration after optic nerve injury. Biochem Biophys Res Commun 514(4):1037-1039 |
| abstractText | 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 3beta (GSK3beta), 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 GSK3beta 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. |
