Effects of Different Concentrations of Oil Mist Particulate Matter on Pulmonary Fibrosis In Vivo and In Vitro

Oil-mist particulate matter (OMPM) refers to oily particles with a small aerodynamic equivalent diameter in ambient air. Since the pathogenesis of pulmonary fibrosis (PF) has not been fully elucidated, this study aims to explore the potential molecular mechanisms of the adverse effects of exposure t...

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Bibliographic Details
Published in:Toxics (Basel) 2022-10, Vol.10 (11), p.647
Main Authors: Nie, Huipeng, Liu, Huanliang, Shi, Yue, Lai, Wenqing, Liu, Xuan, Xi, Zhuge, Lin, Bencheng
Format: Article
Language:English
Subjects:
Animal tissues
Biology
Causes of
Cell differentiation
Cell lines
Collagen (type I)
Cytokines
Differentiation
Drug dosages
E-cadherin
Epithelium
Exposure
Fibroblasts
Fibrosis
Gelatinase A
Health aspects
Histopathology
In vivo methods and tests
Laboratory animals
Lesions
Lubrication and lubricants
Lung diseases
Lungs
MAP kinase
Mist
Molecular modelling
Mortality
N-Cadherin
Oil mist
OMPM
Particles
Particulate emissions
Particulate matter
Pathogenesis
Phenotypes
Pulmonary fibrosis
Pulmonary lesions
Respiratory diseases
Signal transduction
Signaling
Smad3 protein
TGF-β1/MAPK p38
TGF-β1/Smad3
Tissue inhibitor of metalloproteinase 1
Transforming growth factor-b1
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Summary:Oil-mist particulate matter (OMPM) refers to oily particles with a small aerodynamic equivalent diameter in ambient air. Since the pathogenesis of pulmonary fibrosis (PF) has not been fully elucidated, this study aims to explore the potential molecular mechanisms of the adverse effects of exposure to OMPM at different concentrations in vivo and in vitro on PF. In this study, rats and cell lines were treated with different concentrations of OMPM in vivo and in vitro. Sirius Red staining analysis shows that OMPM exposure could cause pulmonary lesions and fibrosis symptoms. The expression of TGF-β1, α-SMA, and collagen I was increased in the lung tissue of rats. The activities of MMP2 and TIMP1 were unbalanced, and increased N-Cadherin and decreased E-Cadherin upon OMPM exposure in a dose-dependent manner. In addition, OMPM exposure could activate the TGF-β1/Smad3 and TGF-β1/MAPK p38 signaling pathways, and the differentiation of human lung fibroblast HFL-1 cells. Therefore, OMPM exposure could induce PF by targeting the lung epithelium and fibroblasts, and activating the TGF-β1/Smad3 and TGF-β1/MAPK p38 signaling pathways.
ISSN:2305-6304
2305-6304
DOI:10.3390/toxics10110647