Time- and dose-resolved proteome of PM2.5 exposure induced lung injury and repair in rat.

In recent years, airborne fine particulate matter (PM2.5) is drawing more public attention due to various of physicochemical features and pathological damages by epidemiological and clinical studies. However, the mechanism of PM2.5-exposure induced lung injury has not been fully characterized. Here, we established a PM2.5-induced rat injury model for short-term and long-term at different concentrations. We employed Fast-seq technique to profile 6,316 proteins and catTFRE approach to profile 387 TFs in lung tissue. In short-term exposure, we elucidated gradually upregulated proteins enriched in response to oxidative stress, phagosome, and ECM-receptor interaction pathway. Long-term exposure mainly showed immune response pathway consisting of increased lymphocytes and cytokines. Intriguingly, we found immune related proteins were recoverable at short-term exposure. During the process of PM2.5 exposure, upregulated proteins presented dose-dependence in lung, including stress response at low-dose, lighter immune response at middle-dose, and severe inflammatory response at high-dose. This dataset provides a rich resource to facilitate the understanding of PM2.5-induced lung damage and repair mechanism.

[1]  Fang Zhang,et al.  The effect of exposure time and concentration of airborne PM2.5 on lung injury in mice: A transcriptome analysis , 2019, Redox biology.

[2]  P. Roepstorff,et al.  TMT-Based Quantitative Proteomics Analysis Reveals Airborne PM2.5-Induced Pulmonary Fibrosis , 2018, International journal of environmental research and public health.

[3]  Zengli Zhang,et al.  Therapeutic potential of bixin in PM2.5 particles‐induced lung injury in an Nrf2‐dependent manner , 2018, Free radical biology & medicine.

[4]  Fabian J Theis,et al.  An atlas of the aging lung mapped by single cell transcriptomics and deep tissue proteomics , 2018, Nature Communications.

[5]  Zhihao Liang,et al.  Comparison and evaluation of two different methods to establish the cigarette smoke exposure mouse model of COPD , 2017, Scientific Reports.

[6]  Xiao-feng Chen,et al.  Exposure to particulate matter 2.5 (PM2.5) induced macrophage‐dependent inflammation, characterized by increased Th1/Th17 cytokine secretion and cytotoxicity , 2017, International immunopharmacology.

[7]  Junchao Duan,et al.  Transcriptomic analyses of human bronchial epithelial cells BEAS-2B exposed to atmospheric fine particulate matter PM2.5. , 2017, Toxicology in vitro : an international journal published in association with BIBRA.

[8]  Peixi Zhang,et al.  Macrophage polarization is related to the pathogenesis of decompression induced lung injury , 2017, Medical gas research.

[9]  Lei Han,et al.  Earthworm extract attenuates silica-induced pulmonary fibrosis through Nrf2-dependent mechanisms , 2016, Laboratory Investigation.

[10]  E. Wouters,et al.  Alteration of canonical and non-canonical WNT-signaling by crystalline silica in human lung epithelial cells. , 2016, Toxicology and applied pharmacology.

[11]  K. He,et al.  Transcriptomic Analyses of the Biological Effects of Airborne PM2.5 Exposure on Human Bronchial Epithelial Cells , 2015, PloS one.

[12]  F. Cheng,et al.  Effects of ambient PM2.5 on pathological injury, inflammation, oxidative stress, metabolic enzyme activity, and expression of c-fos and c-jun in lungs of rats , 2015, Environmental Science and Pollution Research.

[13]  Samantha A. Morris,et al.  CellNet: Network Biology Applied to Stem Cell Engineering , 2014, Cell.

[14]  Deliang Chen,et al.  PM2.5-induced oxidative stress triggers autophagy in human lung epithelial A549 cells. , 2013, Toxicology in vitro : an international journal published in association with BIBRA.

[15]  Jun Qin,et al.  Proteome-wide profiling of activated transcription factors with a concatenated tandem array of transcription factor response elements , 2013, Proceedings of the National Academy of Sciences.

[16]  Or Zuk,et al.  Identification of transcriptional regulators in the mouse immune system , 2013, Nature Immunology.

[17]  Weimin Song,et al.  Effects of ozone and fine particulate matter (PM(2.5)) on rat system inflammation and cardiac function. , 2013, Toxicology letters.

[18]  M. Selbach,et al.  Corrigendum: Global quantification of mammalian gene expression control , 2013, Nature.

[19]  Amin R. Mazloom,et al.  Gene-expression profiles and transcriptional regulatory pathways that underlie the identity and diversity of mouse tissue macrophages , 2012, Nature Immunology.

[20]  Daigo Hashimoto,et al.  Deciphering the transcriptional network of the DC lineage , 2012, Nature Immunology.

[21]  Zhi-Yuan Chen,et al.  Fas/FasL pathway-mediated alveolar macrophage apoptosis involved in human silicosis , 2011, Apoptosis.

[22]  M. Selbach,et al.  Global quantification of mammalian gene expression control , 2011, Nature.

[23]  W. Zin,et al.  Low dose of fine particulate matter (PM2.5) can induce acute oxidative stress, inflammation and pulmonary impairment in healthy mice , 2011, Inhalation toxicology.

[24]  Ariel S. Schwartz,et al.  An Atlas of Combinatorial Transcriptional Regulation in Mouse and Man , 2010, Cell.

[25]  Fabrice Cazier,et al.  Ambient particulate matter (PM2.5): physicochemical characterization and metabolic activation of the organic fraction in human lung epithelial cells (A549). , 2007, Environmental research.

[26]  Weimin Song,et al.  Pulmonary responses to fine particles: differences between the spontaneously hypertensive rats and wistar kyoto rats. , 2007, Toxicology letters.

[27]  J. Chow Health Effects of Fine Particulate Air Pollution: Lines that Connect , 2006, Journal of the Air & Waste Management Association.

[28]  L. Bourguignon,et al.  CD44 interaction with ankyrin and IP3 receptor in lipid rafts promotes hyaluronan-mediated Ca2+ signaling leading to nitric oxide production and endothelial cell adhesion and proliferation. , 2004, Experimental cell research.

[29]  D. Sheppard Functions of pulmonary epithelial integrins: from development to disease. , 2003, Physiological reviews.

[30]  L. Bourguignon,et al.  CD44v10 interaction with Rho-kinase (ROK) activates inositol 1,4,5-triphosphate (IP3) receptor-mediated Ca2+ signaling during hyaluronan (HA)-induced endothelial cell migration. , 2002, Cell motility and the cytoskeleton.

[31]  A. Ledbetter,et al.  The spontaneously hypertensive rat as a model of human cardiovascular disease: evidence of exacerbated cardiopulmonary injury and oxidative stress from inhaled emission particulate matter. , 2000, Toxicology and applied pharmacology.