Genetic inhibition of CRMP2 phosphorylation delays Wallerian degeneration after optic nerve injury
Genetic inhibition of CRMP2 phosphorylation delays Wallerian degeneration after optic nerve injury
复制标题
CRMP2磷酸化的基因抑制可延缓视神经损伤后的沃勒变性
DOI：
10.1016/j.bbrc.2019.05.060
复制
发表时间：
2019
期刊：
影响因子：
--
通讯作者：
Ohshima T
中科院分区：
文献类型：
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作者：
Kinoshita Y;Kondo S;Takahashi K;Nagai J;Wakatsuki S;Araki T;Goshima Y;Ohshima T
轴突变性发生在各种神经系统疾病和创伤性神经损伤的患者中，沃勒变性是损伤后观察到的典型轴突退化现象。崩解素反应介体蛋白2被糖原合成酶ββ磷酸化，参与了视神经损伤后的沃勒变性。我们以前建立了CRMP2基因敲入(CRMP2KI)小鼠系，其中CRMP2被GSK3β的磷酸化被抑制；然而，CRMP2KI小鼠的沃勒变性尚未被检测到。在本研究中，我们检测了CRMP2KI小鼠的视神经沃勒变性是否受到抑制。使用单眼摘除模型，我们基于组织学和生化分析比较了视神经的沃勒变性。我们的实验结果表明，CRMP2磷酸化的遗传抑制延缓了视神经损伤后的沃勒变性。
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 aCRMP2knock-in (CRMP2KI) mouse line, in which CRMP2 phosphorylation by GSK3β is inhibited; however, Wallerian degeneration inCRMP2KI mice has not yet been examined.In this study, we examined whether Wallerian degeneration of the optic nerve is suppressed inCRMP2KI 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.