Department of Ophthalmology, Stem Cell Ocular Regenerative Medicine Center, Wilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Department of Ophthalmology, Stem Cell Ocular Regenerative Medicine Center, Wilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Mol Cell Proteomics. 2021;20:100131. doi: 10.1016/j.mcpro.2021.100131. Epub 2021 Aug 27.
Stress and injury to the retinal pigment epithelium (RPE) often lead to dedifferentiation and epithelial-to-mesenchymal transition (EMT). These processes have been implicated in several retinal diseases, including proliferative vitreoretinopathy, diabetic retinopathy, and age-related macular degeneration. Despite the importance of RPE-EMT and the large body of data characterizing malignancy-related EMT, comprehensive proteomic studies to define the protein changes and pathways underlying RPE-EMT have not been reported. This study sought to investigate the temporal protein expression changes that occur in a human-induced pluripotent stem cell-based RPE-EMT model. We utilized multiplexed isobaric tandem mass tag labeling followed by high-resolution tandem MS for precise and in-depth quantification of the RPE-EMT proteome. We have identified and quantified 7937 protein groups in our tandem mass tag-based MS analysis. We observed a total of 532 proteins that are differentially regulated during RPE-EMT. Furthermore, we integrated our proteomic data with prior transcriptomic (RNA-Seq) data to provide additional insights into RPE-EMT mechanisms. To validate these results, we have performed a label-free single-shot data-independent acquisition MS study. Our integrated analysis indicates both the commonality and uniqueness of RPE-EMT compared with malignancy-associated EMT. Our comparative analysis also revealed that multiple age-related macular degeneration-associated risk factors are differentially regulated during RPE-EMT. Together, our integrated dataset provides a comprehensive RPE-EMT atlas and resource for understanding the molecular signaling events and associated biological pathways that underlie RPE-EMT onset. This resource has already facilitated the identification of chemical modulators that could inhibit RPE-EMT, and it will hopefully aid in ongoing efforts to develop EMT inhibition as an approach for the treatment of retinal disease.
视网膜色素上皮 (RPE) 的应激和损伤通常会导致去分化和上皮-间充质转化 (EMT)。这些过程与几种视网膜疾病有关,包括增生性玻璃体视网膜病变、糖尿病性视网膜病变和年龄相关性黄斑变性。尽管 RPE-EMT 很重要,并且有大量描述与恶性肿瘤相关的 EMT 的数据,但尚未有综合蛋白质组学研究来定义 RPE-EMT 背后的蛋白质变化和途径。本研究旨在调查在基于人诱导多能干细胞的 RPE-EMT 模型中发生的时间性蛋白质表达变化。我们利用多重等重串联质量标签标记,然后进行高分辨率串联 MS,对 RPE-EMT 蛋白质组进行精确和深入的定量分析。在基于串联质谱标签的 MS 分析中,我们鉴定和定量了 7937 个蛋白质组。我们观察到在 RPE-EMT 过程中共有 532 个蛋白质差异调节。此外,我们将蛋白质组学数据与之前的转录组学 (RNA-Seq) 数据进行整合,以提供对 RPE-EMT 机制的更多见解。为了验证这些结果,我们进行了无标签单次数据独立采集 MS 研究。我们的综合分析表明,与恶性肿瘤相关的 EMT 相比,RPE-EMT 既有共性又有独特性。我们的比较分析还表明,多个年龄相关性黄斑变性相关风险因素在 RPE-EMT 过程中差异调节。总之,我们的综合数据集提供了一个全面的 RPE-EMT 图谱和资源,用于了解 RPE-EMT 发生的分子信号事件和相关生物学途径。该资源已经促进了化学调节剂的鉴定,这些调节剂可以抑制 RPE-EMT,并有望帮助正在进行的努力,将 EMT 抑制作为治疗视网膜疾病的一种方法。