Namgung Uk, Choi Bo-Hwa, Park Sehwan, Lee Jung-Uek, Seo Hyung-Suk, Suh Byung-Chang, Kim Kyong-Tai
Department of Life Science, Pohang University of Science and Technology, Pohang 790-784, South Korea.
Mol Cell Neurosci. 2004 Mar;25(3):422-32. doi: 10.1016/j.mcn.2003.11.005.
Cyclin-dependent kinase 5 (Cdk5) is a serine-threonine kinase that is activated by the binding of p35 or p39 regulatory protein. Cdk5 and p35 are highly localized in the growth cone of cultured neurons, and Cdk5 activity is associated with neurite outgrowth. Here we report evidence on the functional involvement of Cdk5 kinase in regenerating peripheral nerve fibers. Elevated levels of Cdk5 protein were found in regenerating axons of facial motor neurons after nerve crush, and Cdk5 kinase activity was increased with a similar time course as increases in Cdk5 protein levels. The p35 protein was also found to be associated with increased Cdk5 activity in regenerating nerves. Administration of Cdk5 inhibitors, roscovitine and olomoucine, into the crushed nerves resulted in decreases in Cdk5 kinase activity in nerves and retardation of nerve fiber regrowth. Retardation of axonal regeneration by Cdk5 inhibition was confirmed by reduced labeling of facial motor neurons using retrograde tracer fluorogold (FG). These findings provide first in vivo evidence indicating that Cdk5 activity, which is induced by axonal injury, may play an important role in axonal regeneration.
细胞周期蛋白依赖性激酶5(Cdk5)是一种丝氨酸 - 苏氨酸激酶,可通过与p35或p39调节蛋白结合而被激活。Cdk5和p35高度定位于培养神经元的生长锥中,并且Cdk5活性与神经突生长相关。在此,我们报告了关于Cdk5激酶在周围神经纤维再生中功能参与的证据。在神经挤压后,在面神经运动神经元的再生轴突中发现Cdk5蛋白水平升高,并且Cdk5激酶活性随时间的增加与Cdk5蛋白水平的增加相似。还发现p35蛋白与再生神经中Cdk5活性的增加有关。将Cdk5抑制剂roscovitine和olomoucine注入挤压的神经中,导致神经中Cdk5激酶活性降低以及神经纤维再生延迟。通过使用逆行示踪剂荧光金(FG)对面神经运动神经元进行标记减少,证实了Cdk5抑制对轴突再生的延迟作用。这些发现提供了首个体内证据,表明由轴突损伤诱导的Cdk5活性可能在轴突再生中起重要作用。