Lin D, Liang Y, Zheng D, Chen Y, Jing X, Lei M, Zeng Z, Zhou T, Wu X, Peng S, Huang K, Yang L, Xiao S, Liu J, Tao E
Department of Neurology, The Sun Yat-sen Memorial Hospital of Sun Yat-sen University, 107 Yanjiang West Road, Guangzhou 510080,China.
Department of Neurology, The Sun Yat-sen Memorial Hospital of Sun Yat-sen University, 107 Yanjiang West Road, Guangzhou 510080,China; Guangdong Province Key Laboratory of Brain Function and Disease, Zhongshan School of Medicine, Sun Yat-sen University, 74 Zhongshan 2nd Road, Guangzhou 510080, China.
Gene. 2018 Mar 20;647:244-260. doi: 10.1016/j.gene.2018.01.023. Epub 2018 Jan 10.
In order to uncover the remarkable pathogenic genes or molecular pathological process in Parkinson's disease (PD), we employed a microarray analysis upon the cellular PD model induced by rotenone. Compared to the control group, 2174 genes were screened out to be expressed differently in the rotenone-induced group by certain criterion. GO analysis and the pathways analysis showed the significant enrichment of genes that were associated with the biological process of cell cycle, apoptotic process, organelle fusion, mitochondrial lesion, endoplasmic reticulum stress and so on. Among these significant DE genes, some were sorted out to be involved in cell cycle and protein processing in endoplasmic reticulum. As the PPI network analysis showed, the interaction relationship of the DEGs involved in the process of protein generation in endoplasmic reticulum(ER) was clearly showed up. As a prediction, we emphasized the genes EDEM1, ATF4, TRAF2 might play central roles in the protein misfolding process during the progression of Parkinson's disease and these new-found genes might be the future research focus and therapeutic targets in PD.
为了揭示帕金森病(PD)中显著的致病基因或分子病理过程,我们对鱼藤酮诱导的细胞性PD模型进行了微阵列分析。与对照组相比,按照一定标准筛选出2174个基因在鱼藤酮诱导组中表达存在差异。基因本体(GO)分析和通路分析表明,与细胞周期、凋亡过程、细胞器融合、线粒体损伤、内质网应激等生物学过程相关的基因显著富集。在这些显著差异表达(DE)基因中,一些被筛选出参与细胞周期和内质网中的蛋白质加工过程。蛋白质-蛋白质相互作用(PPI)网络分析显示,内质网中蛋白质生成过程中涉及的差异表达基因的相互作用关系清晰呈现。作为一种预测,我们强调基因EDEM1、ATF4、TRAF2可能在帕金森病进展过程中的蛋白质错误折叠过程中起核心作用,这些新发现的基因可能是未来帕金森病研究的重点和治疗靶点。