Guo Yinsheng, Ma Yue, Zhang Yanwei, Zhou Li, Huang Suli, Wen Ying, Zou Fei, Cheng Jinquan
Shenzhen Center for Disease Control and Prevention, Shenzhen, 518055, Guangdong, China; Department of Occupational Health and Occupational Medicine, School of Public Health and Tropical Medicine, Southern Medical University, Guangzhou, Guangdong Province, 510515, Guangdong, China.
Shenzhen Center for Disease Control and Prevention, Shenzhen, 518055, Guangdong, China.
Biochem Biophys Res Commun. 2017 Jul 15;489(1):48-55. doi: 10.1016/j.bbrc.2017.05.099. Epub 2017 May 19.
Ischemic stroke (IS) is characterized by high morbidity and poor prognosis. However, the mechanisms of IS induced injury are still poorly understood. The main aim of this study is to explore the role of autophagy in IS. Ten pairs of whole blood samples of IS patients and matched controls were included to select differential expressed genes (DE genes) by autophagy-related functional gene microarray analysis. And then, one hundred and fifty pairs of whole blood samples of IS patients and matched controls were included to validate the DE genes. Moreover, Gene Ontology (GO) analyses and Pathway analyses were also performed based on the DE gene results. Our results indicated that the co-regulation of autophagy and apoptosis took part in IS-induced injuries, and mitochondrial autophagy and apoptosis played a crucial role in this process. Furthermore, lysosome, protein kinase and endopeptidase also participated in IS. These findings clarified the role of mitochondrial autophagy and apoptosis in ischemic stroke and provided more important biomarkers for the prevention diagnosis and therapeutic implications in IS.
缺血性中风（IS）具有高发病率和预后差的特点。然而，IS所致损伤的机制仍知之甚少。本研究的主要目的是探讨自噬在IS中的作用。纳入10对IS患者全血样本及匹配对照，通过自噬相关功能基因微阵列分析筛选差异表达基因（DE基因）。然后，纳入150对IS患者全血样本及匹配对照以验证DE基因。此外，还基于DE基因结果进行了基因本体（GO）分析和通路分析。我们的结果表明，自噬和凋亡的共同调节参与了IS诱导的损伤，线粒体自噬和凋亡在此过程中起关键作用。此外，溶酶体、蛋白激酶和内肽酶也参与了IS。这些发现阐明了线粒体自噬和凋亡在缺血性中风中的作用，并为IS的预防、诊断和治疗意义提供了更重要的生物标志物。
