Role of oxidative stress in Retinitis pigmentosa: new involved pathways by an RNA-Seq analysis (Retracted Article)
Role of oxidative stress in Retinitis pigmentosa: new involved pathways by an RNA-Seq analysis (Retracted Article)
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DOI：
10.1080/15384101.2018.1558873
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发表时间：
2019-01-02
期刊：
影响因子：
4.3
通讯作者：
Sidoti, Antonina
中科院分区：
文献类型：
--
作者：
Donato, Luigi;Scimone, Concetta;Sidoti, Antonina
视网膜色素变性是一种以进行性视网膜裂孔为特征的异质性遗传性眼病。视网膜色素上皮(RPE)是视网膜色素上皮(RPE)变性的主要原因之一，氧化应激抑制了对光感受器的代谢支持。在这里，氧化应激在RP的发生和发展中的作用是通过对人RPE细胞的比较全转录组分析的，在不同的时间点，用100mU g/ml的oxLDL处理和不处理的人RPE细胞。实验重复三次，并在离子质子(TM)测序系统上进行。数据分析，包括低质量的读数修剪和基因表达的量化，通过CLC基因组学工作台软件实现。整个分析突出了14个聚集的“宏观途径”和许多子途径，根据对5271个表达变化最大的基因的选择进行分类。其中23个基因是已知的RP致病基因(15个高表达，8个低表达)，它们的浓缩和交叉分析突出了新的77个候选相关基因(49个高表达，28个低表达)。最后的过滤分析突出了29个候选基因。这些数据表明，许多尚未与RP相关的新基因可能会影响其发病机制。
Retinitis pigmentosa (RP) is a very heterogeneous inherited ocular disorder group characterized by progressive retinal disruption. Retinal pigment epithelium (RPE) degeneration, due to oxidative stress which arrests the metabolic support to photoreceptors, represents one of the principal causes of RP. Here, the role of oxidative stress in RP onset and progression was analyzed by a comparative whole transcriptome analysis of human RPE cells, treated with 100 mu g/ml of oxLDL and untreated, at different time points. Experiment was thrice repeated and performed on Ion Proton(TM) sequencing system. Data analysis, including low quality reads trimming and gene expression quantification, was realized by CLC Genomics Workbench software. The whole analysis highlighted 14 clustered "macro-pathways" and many sub-pathways, classified by selection of 5271 genes showing the highest alteration of expression. Among them, 23 genes were already known to be RP causative ones (15 over-expressed and 8 down-expressed), and their enrichment and intersection analyses highlighted new 77 candidate related genes (49 over-expressed and 28 down-expressed). A final filtering analysis then highlighted 29 proposed candidate genes. This data suggests that many new genes, not yet associated with RP, could influence its etiopathogenesis.