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iTRAQ based proteomic analysis of PM2.5 induced lung damage

机译：基于iTRAQ的PM2.5诱导的肺损伤的蛋白质组学分析

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Haze pollution has become a global environmental problem, subsequently affecting air quality, climate, economy and human health. Notably, PM _(2.5) (particulate matter with an aerodynamic diameter less than 2.5 micrometers) significantly accounts for a variety of adverse health effects, in particular pulmonary diseases such as asthma and lung cancer. Clinical diagnosis and medical treatment of the lung damage caused by PM _(2.5) still remain significant challenges due to the lack of specific biomarkers and pathways. Here, we established a rat model of nonsurgical intratracheal instillation to investigate PM _(2.5) exposure and employed iTRAQ based analytical technique and bioinformatics tools to identify putative biomarkers and pathways. We identified 163 differentially expressed proteins (DEPs). Among these proteins, we screened six DEPs (HMOX1, MP2K5, XRCC1 E9PTZ7, KNT2 and A1AG) as the putative biomarkers, with significant differentially expressed levels (percentage increment > 140%). Pathway analysis indicated that calcium signaling, MAPK and PI3K/AKT might be involved in the process of PM _(2.5) -induced lung damage. Western-blotting was used to verify DEPs in the AEC-II cell model for early diagnosis. In summary, our data can serve as fundamental research clues for further studies of PM _(2.5) -induced toxicity in the lungs.
机译：霾污染已经成为全球性的环境问题，随后影响到空气质量，气候，经济和人类健康。值得注意的是，PM _（2.5）（空气动力学直径小于2.5微米的颗粒物）显着说明了多种不利健康影响，尤其是肺部疾病，例如哮喘和肺癌。由于缺乏特定的生物标志物和途径，由PM _（2.5）引起的肺损伤的临床诊断和医学治疗仍然是重大挑战。在这里，我们建立了非手术气管内滴注大鼠模型以研究PM _（2.5）暴露，并采用了基于iTRAQ的分析技术和生物信息学工具来确定推定的生物标志物和途径。我们确定了163个差异表达蛋白（DEP）。在这些蛋白质中，我们筛选了六个DEP（HMOX1，MP2K5，XRCC1 E9PTZ7，KNT2和A1AG）作为推定的生物标志物，它们的表达水平差异显着（百分增量> 140％）。通路分析表明，钙信号，MAPK和PI3K / AKT可能参与了PM_（2.5）诱导的肺损伤。 Western-blotting用于验证AEC-II细胞模型中的DEP，以进行早期诊断。总之，我们的数据可作为进一步研究PM _（2.5）诱导的肺毒性的基础研究线索。

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