Department of Biochemistry, Molecular Biology, and Biophysics, College of Biological Sciences and.
Division of Environmental and Occupational Health Sciences, National Jewish Health, Denver, Colorado.
Am J Respir Cell Mol Biol. 2020 Dec;63(6):727-738. doi: 10.1165/rcmb.2020-0070PS.
Sarcoidosis is a multisystem disease with heterogeneity in manifestations and outcomes. System-level studies leveraging "omics" technologies are expected to define mechanisms contributing to sarcoidosis heterogeneous manifestations and course. With improvements in mass spectrometry (MS) and bioinformatics, it is possible to study protein abundance for a large number of proteins simultaneously. Contemporary fast-scanning MS enables the acquisition of spectral data for deep coverage of the proteins with data-dependent or data-independent acquisition MS modes. Studies leveraging MS-based proteomics in sarcoidosis have characterized BAL fluid (BALF), alveolar macrophages, plasma, and exosomes. These studies identified several differentially expressed proteins, including protocadherin-2 precursor, annexin A2, pulmonary surfactant A2, complement factors C3, vitamin-D-binding protein, cystatin B, and amyloid P, comparing subjects with sarcoidosis with control subjects. Other studies identified ceruloplasmin, complement factors B, C3, and 1, and others with differential abundance in sarcoidosis compared with other interstitial lung diseases. Using quantitative proteomics, most recent studies found differences in PI3K/Akt/mTOR, MAP kinase, pluripotency-associated transcriptional factor, and hypoxia response pathways. Other studies identified increased clathrin-mediated endocytosis and Fcγ receptor-mediated phagocytosis pathways in sarcoidosis alveolar macrophages. Although studies in mixed BAL and blood cells or plasma are limited, some of the changes in lung compartment are detected in the blood cells and plasma. We review proteomics for sarcoidosis with a focus on the existing MS data acquisition strategies, bioinformatics for spectral data analysis to infer protein identity and quantity, unique aspects about biospecimen collection and processing for lung-related proteomics, and proteomics studies conducted to date in sarcoidosis.
结节病是一种多系统疾病,其临床表现和结局存在异质性。利用“组学”技术进行系统水平的研究有望确定导致结节病表现和病程异质性的机制。随着质谱(MS)和生物信息学的改进,现在可以同时研究大量蛋白质的蛋白质丰度。现代快速扫描 MS 能够以数据依赖或数据独立采集 MS 模式获取深度覆盖蛋白质的光谱数据。利用基于 MS 的蛋白质组学研究结节病的研究已经对 BAL 液(BALF)、肺泡巨噬细胞、血浆和外泌体进行了描述。这些研究鉴定了几种差异表达的蛋白质,包括原钙黏蛋白-2 前体、膜联蛋白 A2、肺表面活性剂 A2、补体因子 C3、维生素 D 结合蛋白、胱抑素 B 和淀粉样蛋白 P,将结节病患者与对照者进行比较。其他研究鉴定了铜蓝蛋白、补体因子 B、C3 和 1,以及与其他间质性肺疾病相比在结节病中丰度差异的其他蛋白。使用定量蛋白质组学,最近的研究发现 PI3K/Akt/mTOR、MAP 激酶、多能性相关转录因子和低氧反应途径存在差异。其他研究鉴定了结节病肺泡巨噬细胞中网格蛋白介导的内吞作用和 Fcγ 受体介导的吞噬作用途径增加。尽管混合 BAL 和血细胞或血浆的研究有限,但在血液细胞和血浆中检测到一些肺隔室的变化。我们综述了结节病的蛋白质组学,重点介绍了现有的 MS 数据采集策略、光谱数据分析的生物信息学,以推断蛋白质的身份和数量、与肺部相关的蛋白质组学生物样本采集和处理的独特方面,以及迄今为止在结节病中进行的蛋白质组学研究。