Miller Renee M, Callahan Linda M, Casaceli Cindy, Chen Linlin, Kiser Gretchen L, Chui Buena, Kaysser-Kranich Tamma M, Sendera Timothy J, Palaniappan Chockalingam, Federoff Howard J
Center for Aging and Developmental Biology, Aab Institute of Biomedical Sciences, University of Rochester, Rochester, New York 14642, USA.
J Neurosci. 2004 Aug 25;24(34):7445-54. doi: 10.1523/JNEUROSCI.4204-03.2004.
Parkinson's disease pathogenesis proceeds through several phases, culminating in the loss of dopaminergic neurons of the substantia nigra (SN). Although the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of oxidative SN injury is frequently used to study degeneration of dopaminergic neurons in mice and non-human primates, an understanding of the temporal sequence of molecular events from inhibition of mitochondrial complex 1 to neuronal cell death is limited. Here, microarray analysis and integrative data mining were used to uncover pathways implicated in the progression of changes in dopaminergic neurons after MPTP administration. This approach enabled the identification of small, yet consistently significant, changes in gene expression within the SN of MPTP-treated animals. Such an analysis disclosed dysregulation of genes in three main areas related to neuronal function: cytoskeletal stability and maintenance, synaptic integrity, and cell cycle and apoptosis. The discovery and validation of these alterations provide molecular evidence for an evolving cascade of injury, dysfunction, and cell death.
帕金森病的发病机制经历几个阶段,最终导致黑质(SN)多巴胺能神经元的丧失。尽管1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的黑质氧化损伤模型常用于研究小鼠和非人类灵长类动物中多巴胺能神经元的变性,但对于从线粒体复合物1受抑制到神经元细胞死亡这一分子事件的时间顺序,人们的了解还很有限。在此,我们利用微阵列分析和综合数据挖掘来揭示MPTP给药后多巴胺能神经元变化进程中涉及的信号通路。这种方法能够识别MPTP处理动物黑质内基因表达的微小但始终显著的变化。这样的分析揭示了与神经元功能相关的三个主要领域的基因失调:细胞骨架稳定性与维持、突触完整性以及细胞周期与凋亡。这些改变的发现和验证为损伤、功能障碍和细胞死亡的不断演变的级联反应提供了分子证据。