scholarly journals Diesel Exhaust Particles Activate the Matrix-Metalloproteinase-1 Gene in Human Bronchial Epithelia in a ß-Arrestin-Dependent Manner via Activation of RAS

2008 ◽  
Author(s):  
Jinju Li ◽  
Andrew J. Ghio ◽  
Seung-Hyun Cho ◽  
Constance E. Brinckerhoff ◽  
Sidney A. Simon ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Diesel Exhaust ◽  
Diesel Exhaust Particles ◽  
Dependent Manner ◽  
Matrix Metalloproteinase 1 ◽  
Bronchial Epithelia ◽  
The Matrix ◽  
Exhaust Particles

scholarly journals TRPV4-Mediated Calcium Influx into Human Bronchial Epithelia upon Exposure to Diesel Exhaust Particles

2011 ◽  
Vol 119 (6) ◽  
pp. 784-793 ◽  
Author(s):  
Jinju Li ◽  
Patrick Kanju ◽  
Michael Patterson ◽  
Wei-Leong Chew ◽  
Seung-Hyun Cho ◽  
...  
Keyword(s):  
Diesel Exhaust ◽  
Calcium Influx ◽  
Diesel Exhaust Particles ◽  
Bronchial Epithelia ◽  
Exhaust Particles

scholarly journals Determination of Genotoxicity Attributed to Diesel Exhaust Particles in Normal Human Embryonic Lung Cell (WI-38) Line

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 291
Author(s):  
Joong Won Lee ◽  
Hee Jae Lee ◽  
Young-Joo Lee ◽  
Yong-beom Lim ◽  
Woo Jong Sim ◽  
...  
Keyword(s):  
Dna Damage ◽  
Differentially Expressed Genes ◽  
Diesel Exhaust ◽  
Human Lung ◽  
Diesel Exhaust Particles ◽  
Differentially Expressed ◽  
Dependent Manner ◽  
Dna Breaks ◽  
Normal Human ◽  
Exhaust Particles

Several epidemiological studies concluded that inhalation of diesel exhaust particles (DEP) is associated with an increase in the relative risk of lung cancer. In vitro research evaluating the genetic damage and/or changes in gene expression have been attempted to explain the relationship between DEP exposure and carcinogenicity. However, to date, investigations have been largely confined to studies in immortalized or tumorigenic epithelial cell models. Few studies have investigated damage at the chromosomal level to DEP exposure in normal cell lines. Here, we present the genotoxic effects of DEP in normal cells (embryonic human lung fibroblasts) by conventional genotoxicity testing (micronuclei (MN) and comet assay). We show the differentially expressed genes and enriched pathways in DEP-exposed WI-38 cells using RNA sequencing data. We observed a significant increase in single-strand DNA breaks and the frequency of MN in DEP-exposed cells in a dose-dependent manner. The differentially expressed genes following DEP exposure were significantly enriched in the pathway for responding to xenobiotics and DNA damage. Taken together, these results show that DEP exposure induced DNA damage at the chromosomal level in normal human lung cells and provide information on the expression of genes associated with genotoxic stress.

Cardiovascular and lung inflammatory effects induced by systemically administered diesel exhaust particles in rats

2007 ◽  
Vol 292 (3) ◽  
pp. L664-L670 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Sultan Al-Maskari ◽  
Badreldin H. Ali ◽  
Issa S. Al-Amri
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Diesel Exhaust ◽  
Ultrafine Particles ◽  
Blood Platelet ◽  
Diesel Exhaust Particles ◽  
Lung Edema ◽  
Dependent Manner ◽  
Exhaust Particles

Pollution by particulates has consistently been associated with increased cardiorespiratory morbidity and mortality. It has been suggested that ultrafine particles, of which diesel exhaust particles (DEP) are significant contributors, are able to translocate from the airways into the bloodstream in vivo. In the present study, we assessed the effect of systemic administration of DEP on cardiovascular and respiratory parameters. DEP were administered into the tail vein of rats, and heart rate, blood pressure, blood platelet activation, and lung inflammation were studied 24 h later. Doses of 0.02, 0.1, or 0.5 mg DEP/kg (8, 42, or 212 μg DEP/rat) induced a significant decrease of heart rate and blood pressure compared with saline-treated rats. Although the number of platelets was not affected, all the doses of DEP caused a shortening of the bleeding time. Similarly, in addition to triggering lung edema, the bronchoalveolar lavage analysis revealed the presence of neutrophil influx in DEP-treated rats in a dose-dependent manner. We conclude that the presence of DEP in the systemic circulation leads not only to cardiovascular and haemostatic changes but it also triggers pulmonary inflammation.

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