Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Differentially expressed genes related to inflammatory disease on nasal cavity induced by diesel exhaust particles (DEPs)

ABSTRACT: Recently air pollution has become serious environmental issues effect. Contaminated air by pollutants, such as emission of diesel fuel, enter the human body through airway tract and can cause inflammatory diseases in respiratory system. The relation between air pollutant and development of respiratory diseases have well-studied, but the processes of disease outbreak were not fully studied yet. We investigated global gene expression induced by diesel exhaust particle (DEP), one of air pollutants in primary human nasal epithelial cell (PHNEC) with the purpose of identifying potential biomarkers. Furthermore, we analyzed signaling pathway among differentially expressed genes (DEGs) for elucidating signaling networks of process developing airway diseases. Consequentially, we suggested several key biomarkers that include not only the expression changes but also the meaning of relation between genes. This findings might be used for early diagnosis and prevention of upper respiratory disease, especially rhinitis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE102304 | GEO | 2017/12/31

SECONDARY ACCESSION(S): PRJNA397382

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptomic Changes in the Nasal Epithelium Associated with Diesel Engine Exhaust Exposure

Project description:Diesel engine exhaust (DEE) is one of the major contributors to air pollution around the world, and exposure to DEE is associated with lung cancer and other airway diseases. Although recent studies have investigated the effects of exposure to DEE, the mechanisms by which it leads to lung cancer pathogenesis are not well understood. We have previously investigated the transcriptomic changes that occur due to exposure to cigarette smoke and burning of bituminous (smoky) as well as anthracite (smokeless) coal in the airway epithelium, and in this study we assess the gene expression alterations in the nasal epithelium that are associated with chronic DEE exposure of diesel engine factory workers to better understand which molecular changes may lead to pathogenesis of lung cancer.

2019-12-19 | GSE124267 | GEO

Identification of novel potential biomarkers and signaling pathways related to otitis media induced by diesel exhaust particle in in vivo system via transcriptomic analysis

Project description:Association between air pollutants and inflammatory diseases such as Otitis Media (OM) has been shown in recent studies. Indeed, significantly higher rates of OM incidence in air polluted area have been evident by epidemiological researchers. Diesel exhaust particle (DEP), one of major components among diverse air pollutants, is characterized by a carbonic mixture composed of polycyclic aromatic hydrocarbons (PAHs), nitro-PAHs, small amounts of sulfate, nitrate, metals, and other trace elements. The exposure to DEP as a risk factor for inflammatory diseases has been reported in several recent investigations. In line with these, our previous study identified potential biomarkers in in vitro system through gene expression microarray and pathway analysis. Although investigations in in vitro system have been conducted to elucidate plausible biomarkers and molecular mechanisms related with DEP, it is necessary to carry out in vivo study to identify exact biological relevance regarding incidence of OM caused by DEP exposure. In this study, we discovered potential molecular biomarkers and pathways triggered by DEP exposure in rodent model. Here, we conducted transcriptomic analysis to identify novel potential biomarkers in middle ears of DEP-exposed mice. A total of 697 genes were differentially expressed in the DEP-exposed mice; 424 genes and 273 genes were up-and down-regulated, respectively. In addition, signaling pathways among differentially expressed genes mediated by DEP exposure were predicted from different two point of view. Subsequently, we identified several key molecular biomarkers, CHRM1, EPO, SOS1, ESR1, CD4, and IFNA1. In conclusion, our results might ascertain related cell process and signaling interacted genes underlying DEP exposure and its effects. Moreover, the discovered biomarkers can be recognized as potential candidates for developing early diagnosis and effective treatment strategies of DEP-mediated disorders.

2016-09-13 | GSE86844 | GEO

DNA methylation changes in A549 cells after four weeks of exposure to 30 μg/ml diesel exhaust particles.

Project description:Diesel exhaust particles (DEP), which contain hazardous compounds, are emitted during the combustion of diesel. As approximately one-third of the vehicles worldwide use diesel, there are growing concerns on the risks posed by DEP to human health. Long-term exposure to DEP is associated with airway hyperresponsiveness, pulmonary fibrosis, and inflammation; however, the molecular mechanisms behind the effects of DEP on the respiratory tract are poorly understood. Such mechanisms can be addressed by examining transcriptional and DNA methylation changes. In this study, we investigated the effect of 4 weeks exposure to 30 μg/ml DEP on DNA methylation levels in A549 cells.

2024-08-05 | GSE267215 | GEO

Transcriptional changes in A549 cells after four weeks of exposure to 30 μg/ml diesel exhaust particles measured by RNA-seq.

2024-08-05 | GSE267213 | GEO

Identification of a dose of diesel exhaust particles that is sufficient to induce significant DNA methylation changes in A549 cells after four weeks of exposure.

Project description:Diesel exhaust particles (DEP), which contain hazardous compounds, are emitted during the combustion of diesel. As approximately one-third of the vehicles worldwide use diesel, there are growing concerns on the risks posed by DEP to human health. Long-term exposure to DEP is associated with airway hyperresponsiveness, pulmonary fibrosis, and inflammation; however, the molecular mechanisms behind the effects of DEP on the respiratory tract are poorly understood. Such mechanisms can be addressed by examining transcriptional and DNA methylation changes. In this study, we investigated DEP dose sufficient to induce significant DNA methylation changes after four weeks of exposure.

2024-08-05 | GSE267214 | GEO

Transcriptional changes in A549 cells after four weeks of exposure to 30 μg/ml diesel exhaust particles measured by Agilent SurePrint G3 Human Gene Expression Microarray.

2024-08-05 | GSE267216 | GEO

Proteomic analysis reveals activation of platelet- and fibrosis-related pathways in hearts of ApoE-/- mice exposed to diesel exhaust particles

Project description:Air pollution is an environmental risk factor linked to multiple human diseases including cardiovascular diseases (CVDs). While particulate matter (PM) emitted by diesel exhaust damages multiple organ systems, heart disease is one of the most severe pathologies affected by PM. However, the in vivo effects of diesel exhaust particles (DEP) on the heart and the molecular mechanisms of DEP-induced heart dysfunction have not been investigated. In the current study, we attempted to identify the proteomic signatures of heart fibrosis caused by diesel exhaust particles (DEP) in CVDs-prone apolipoprotein E knockout (ApoE-/-) mice model using tandem mass tag (TMT)-based quantitative proteomic analysis. DEP exposure induced mild heart fibrosis in ApoE-/- mice compared with severe heart fibrosis in ApoE-/- mice that were treated with CVDs-inducing peptide, angiotensin II. TMT-based quantitative proteomic analysis of heart tissues between PBS- and DEP-treated ApoE-/- mice revealed significant upregulation of proteins associated with platelet activation and TGFβ-dependent pathways. Our data suggest that DEP exposure could induce heart fibrosis, potentially via platelet-related pathways and TGFβ induction, causing cardiac fibrosis and dysfunction.

2023-12-09 | PXD045029 | Pride

Lung cell responses to ship diesel exhaust particles

Project description:Human BEAS-2B bronchial epithelial cells were exposed directly at the air-liquid interphase towards exhaust gas and particles of a ship engine. The goal was to compare the responses towards different fuel combustions. The engine run either on diesel fuel (DF) or on Heavy Fuel Oil (HFO).

2015-02-01 | GSE63962 | GEO

Pooled 2D LC-MS of the bronchial secretome under exposure to diesel exhaust, allergen, and mixture of both irritants

Project description:Four 2D LC-MS runs of pooled BALF (brochanial lavage fluid) from 5 study participants, each representing a different controlled exposure: balf2dg2=filtered air/saline; balf2dg1=allergen, balf2dg3=diesel, balf2dg4=allergen+diesel mixture.

2017-05-25 | MSV000081110 | MassIVE

Diesel exhaust and house dust mite allergen lead to common changes in the airway methylome and hydroxymethylome

Project description:Genomewide DNA methylation profiling of saline, diesel exhaust particiles and house dust mite treated human airway epithelial cells. Methylation profiles were generated by the Illumina Infinium MethylationEPIC beadchips.

2018-12-31 | GSE116402 | GEO