TMT-Based Quantitative Proteomics Analysis Reveals Airborne PM 2.5 -Induced Pulmonary Fibrosis

Shan Liu, Wei Zhang, Fang Zhang, Peter Roepstorff, Fuquan Yang, Zhongbing Lu and Wenjun Ding
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Shan Liu: Laboratory of Environment and Health, College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China
Wei Zhang: Laboratory of Environment and Health, College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China
Fang Zhang: Laboratory of Environment and Health, College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China
Peter Roepstorff: Department of Biochemistry and Molecular Biology, University of Southern Denmark, DK-5230 Odense M, Denmark
Fuquan Yang: National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China
Zhongbing Lu: Laboratory of Environment and Health, College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China
Wenjun Ding: Laboratory of Environment and Health, College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China

IJERPH, 2018, vol. 16, issue 1, 1-14

Abstract: Epidemiological and experimental studies have documented that long-term exposure to fine particulate matter (PM 2.5 ) increases the risk of respiratory diseases. However, the details of the underlying mechanism remain unclear. In this study, male C57BL/6 mice were exposed to ambient PM 2.5 (mean daily concentration ~64 µg/m 3 ) for 12 weeks through a “real-world” airborne PM 2.5 exposure system. We found that PM 2.5 caused severe lung injury in mice as evidenced by histopathological examination. Then, tandem mass tag (TMT) labeling quantitative proteomic technology was performed to analyze protein expression profiling in the lungs from control and PM 2.5 -exposed mice. A total of 32 proteins were differentially expressed in PM 2.5 -exposed lungs versus the controls. Among these proteins, 24 and 8 proteins were up- and down-regulated, respectively. Gene ontology analysis indicated that PM 2.5 exerts a toxic effect on lungs by affecting multiple biological processes, including oxidoreductase activity, receptor activity, and protein binding. Furthermore, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that extracellular matrix (ECM)–receptor interaction, phagosome, small cell lung cancer, and phosphatidylinositol 3-kinase(PI3K)-protein kinase B (Akt) signaling pathways contribute to PM 2.5 -induced pulmonary fibrosis. Taken together, these results provide a comprehensive proteomics analysis to further understanding of the molecular mechanisms underlying PM 2.5 -elicited pulmonary disease.

Keywords: particulate matter (PM 2.5 ); pulmonary fibrosis; toxicity; quantitative proteomics (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2018
References: View complete reference list from CitEc
Citations: View citations in EconPapers (1)

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