Activation of Ca2+/calmodulin-dependent protein kinase II α in the spinal cords of rats with clip compression injury
Activation of Ca2+/calmodulin-dependent protein kinase II α in the spinal cords of rats with clip compression injury
复制标题
DOI：
10.1016/j.brainres.2009.03.032
复制
发表时间：
2009-05-19
期刊：
影响因子：
2.9
通讯作者：
Moon, Chanjong
中科院分区：
文献类型：
--
作者：
Song, Myoung-Sub;Seo, Heung-Sik;Moon, Chanjong
Ca2+/钙调蛋白依赖性蛋白激酶 II α (CaMKII α) 在中枢神经系统中含量丰富，在调节神经元可塑性和存活中发挥重要作用。然而，CaMKII α 激活在脊髓创伤中的作用仍不清楚。本研究探讨了夹子压缩损伤对磷酸化 CaMKII α (pCaMKII α) 水平及其在大鼠脊髓中细胞定位的影响。蛋白质印迹分析显示，损伤部位的头侧（受伤后第 7、14 和 21 天）和尾侧（受伤后第 4、7、14 和 21 天）区域的 pCaMKII α 水平是未受伤对照的两倍以上。免疫组织化学检查揭示了 pCaMKII α 在正常脊髓对照的背角浅层和神经元中的组成性定位。脊髓损伤后，距脊髓损伤中心约 3 毫米的头侧和尾侧区域，相同成分的水平显着增加。然而，pCaMKII α 在受损脊髓的炎症细胞中非常罕见。在该动物模型中，CaMKII α 可能在脊髓功能障碍的自发逆转中发挥重要作用，从而恢复运动活动，可能是通过重建突触传递和保护神经元免受脊髓损伤发挥作用。 (C) 2009 Elsevier B.V. 保留所有权利。
Ca2+/calmodulin-dependent protein kinase II alpha (CaMKII alpha) is abundant in the central nervous system, where it plays important roles in regulating neuronal plasticity and survival. However, the role of CaMKII alpha activation in traumatically injured spinal cords remains unclear. This study examined the effects of clip compression injury on levels of phosphorylated CaMKII alpha (pCaMKII alpha) and its cellular localization in rat spinal cords. Western blot analysis showed that the pCaMKII alpha levels in both rostral (days 7, 14, and 21 post-injury) and caudal (days 4, 7, 14, and 21 post-injury) areas of the injury site were more than twice the levels in the non-injured controls. Immunohistochemical examination revealed constitutive localization of pCaMKII alpha in the superficial lamina of the dorsal horn and neurons in normal spinal cord controls. After spinal cord injury, levels of the same components were markedly increased in both rostral and caudal regions similar to 3 mm from the center of the spinal cord lesions. However, pCaMKII alpha was very rare in inflammatory cells in the injured spinal cords. in this animal model, CaMKII alpha may play an important role in the spontaneous reversal of spinal cord dysfunction, thus restoring locomotor activity, possibly by functioning in the reconstruction of synaptic transmission and in protecting neurons from spinal cord injury. (C) 2009 Elsevier B.V. All rights reserved.