Di Giovanni Simone, Faden Alan I, Yakovlev Alexander, Duke-Cohan Jonathan S, Finn Tom, Thouin Melissa, Knoblach Susan, De Biase Andrea, Bregman Barbara S, Hoffman Eric P
Department of Neuroscience, Georgetown University Medical Center, Washington, DC, USA.
FASEB J. 2005 Jan;19(1):153-4. doi: 10.1096/fj.04-2694fje. Epub 2004 Nov 2.
Functional recovery after spinal cord injury (SCI) may result in part from axon outgrowth and related plasticity through coordinated changes at the molecular level. We employed microarray analysis to identify a subset of genes the expression patterns of which were temporally coregulated and correlated to functional recovery after SCI. Steady-state mRNA levels of this synchronously regulated gene cluster were depressed in both ventral and dorsal horn neurons within 24 h after injury, followed by strong re-induction during the following 2 wk, which paralleled functional recovery. The identified cluster includes neuritin, attractin, microtubule-associated protein 1a, and myelin oligodendrocyte protein genes. Transcriptional and protein regulation of this novel gene cluster was also evaluated in spinal cord tissue and in single neurons and was shown to play a role in axonal plasticity. Finally, in vitro transfection experiments in primary dorsal root ganglion cells showed that cluster members act synergistically to drive neurite outgrowth.
脊髓损伤（SCI）后的功能恢复可能部分源于轴突生长以及通过分子水平的协调变化产生的相关可塑性。我们采用微阵列分析来鉴定一组基因，其表达模式在时间上受到共同调节且与脊髓损伤后的功能恢复相关。在损伤后24小时内，这个同步调节的基因簇的稳态mRNA水平在腹角和背角神经元中均降低，随后在接下来的2周内强烈重新诱导，这与功能恢复并行。鉴定出的基因簇包括神经生长素、吸引素、微管相关蛋白1a和髓鞘少突胶质细胞蛋白基因。还在脊髓组织和单个神经元中评估了这个新基因簇的转录和蛋白质调节，结果表明其在轴突可塑性中发挥作用。最后，在原代背根神经节细胞中进行的体外转染实验表明，基因簇成员协同作用以驱动神经突生长。
