Resnick Daniel K, Schmitt Caroline, Miranpuri Gurwattan S, Dhodda Vinay K, Isaacson Jason, Vemuganti Raghu
Department of Neurological Surgery, University of Wisconsin, K4/834 Clinical Science Center, 600 Highland Avenue, Madison, WI 53792, USA.
Neuroreport. 2004 Apr 9;15(5):837-9. doi: 10.1097/00001756-200404090-00020.
Investigations into the genetic basis of neuronal damage following spinal cord injury have thus far been limited to the acute phase after the injury. Using microarray analysis, the present study compared the spinal-cord-injury-induced gene expression changes in adult rats at the epicenter and rostral segments of spinal cord at acute (12 h) and delayed (42 days) time points. We have previously reported that the acute response to spinal cord injury involves alterations in genes responsible for inflammation, cell cycle alteration, and altered receptor function. In contrast, the delayed response includes changes in the expression of HSP27, MAG, MAP-2, IGF-1 and ApoE. The alteration in expression of these genes suggests an ongoing repair process in animals whose functional recovery has reached a plateau.
迄今为止，对脊髓损伤后神经元损伤的遗传基础的研究仅限于损伤后的急性期。本研究采用微阵列分析，比较了成年大鼠在脊髓损伤后急性（12小时）和延迟（42天）时间点，脊髓损伤在脊髓损伤中心和头端节段诱导的基因表达变化。我们之前曾报道，对脊髓损伤的急性反应涉及负责炎症、细胞周期改变和受体功能改变的基因的变化。相比之下，延迟反应包括HSP27、MAG、MAP-2、IGF-1和ApoE表达的变化。这些基因表达的改变表明，在功能恢复已达到平台期的动物中，正在进行修复过程。
