Lanzillotta Chiara, Greco Viviana, Valentini Diletta, Villani Alberto, Folgiero Valentina, Caforio Matteo, Locatelli Franco, Pagnotta Sara, Barone Eugenio, Urbani Andrea, Di Domenico Fabio, Perluigi Marzia
Department of Biochemical Sciences "A. Rossi Fanelli", Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Sapienza University of Rome, 00185 Rome, Italy.
Department of Basic Biotechnological Sciences, Intensivological and Perioperative Clinics, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.
Antioxidants (Basel). 2020 Nov 11;9(11):1112. doi: 10.3390/antiox9111112.
Down syndrome (DS) is the most common chromosomal disorder and the leading genetic cause of intellectual disability in humans, which results from the triplication of chromosome 21. To search for biomarkers for the early detection and exploration of the disease mechanisms, here, we investigated the protein expression signature of peripheral blood mononuclear cells (PBMCs) in DS children compared with healthy donors (HD) by using an in-depth label-free shotgun proteomics approach. Identified proteins are found associated with metabolic pathways, cellular trafficking, DNA structure, stress response, cytoskeleton network, and signaling pathways. The results showed that a well-defined number of dysregulated pathways retain a prominent role in mediating DS pathological features. Further, proteomics results are consistent with published study in DS and provide evidences that increased oxidative stress and the increased induction of stress related response, is a participant in DS pathology. In addition, the expression levels of some key proteins have been validated by Western blot analysis while protein carbonylation, as marker of protein oxidation, was investigated. The results of this study propose that PBMCs from DS children might be in an activated state where endoplasmic reticulum stress and increased production of radical species are one of the primary events contributing to multiple DS pathological features.
唐氏综合征(DS)是最常见的染色体疾病,也是人类智力残疾的主要遗传原因,它由21号染色体三体所致。为了寻找用于疾病早期检测和机制探索的生物标志物,在此,我们采用深度无标记鸟枪法蛋白质组学方法,研究了唐氏综合征患儿外周血单个核细胞(PBMC)与健康供体(HD)相比的蛋白质表达特征。鉴定出的蛋白质与代谢途径、细胞运输、DNA结构、应激反应、细胞骨架网络和信号通路相关。结果表明,一定数量明确的失调途径在介导唐氏综合征病理特征方面发挥着重要作用。此外,蛋白质组学结果与已发表的唐氏综合征研究一致,并提供证据表明氧化应激增加以及应激相关反应的诱导增加是唐氏综合征病理过程的参与者。此外,一些关键蛋白质的表达水平已通过蛋白质免疫印迹分析得到验证,同时对作为蛋白质氧化标志物的蛋白质羰基化进行了研究。本研究结果表明,唐氏综合征患儿的外周血单个核细胞可能处于激活状态,其中内质网应激和自由基产生增加是导致多种唐氏综合征病理特征的主要事件之一。