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Acrolein-mediated changes in HUVEC miRNA

ABSTRACT: Acrolein is a major reactive component of vehicle exhaust, cigarette and wood smoke. It is also present in several food substances and is generated endogenously during inflammation and lipid peroxidation. Although previous studies have shown that dietary or inhalation exposure to acrolein results in endothelial activation, platelet activation and accelerated atherogenesis, the basis for these effects is unknown. Moreover, the effects of acrolein on microRNA (miRNA) have not been studied. Using AGILENT miRNA microarray high throughput technology, we have thus characterized the effects of acrolein exposure on miRNA expression in human umbilical vein endothelial cells (HUVEC).

ORGANISM(S): Homo sapiens

PROVIDER: GSE56782 | GEO | 2014/06/03

SECONDARY ACCESSION(S): PRJNA244579

REPOSITORIES: GEO

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Project description:Exposure to traffic-related pollutants, including diesel exhaust, is associated with increased risk of cardiopulmonary disease and mortality; however, the precise biochemical pathways underlying these effects are not known. To investigate biological response mechanisms underlying exposure to traffic related pollutants, we used an integrated molecular response approach that included high-resolution metabolomic profiling and peripheral blood gene expression to identify biological responses to diesel exhaust exposure. Plasma samples were collected from 73 non-smoking males employed in the US trucking industry between February 2009 and October 2010 and analyzed using untargeted high-resolution metabolomics to characterize association with shift- and week-averaged levels of elemental carbon (EC), organic carbon (OC) and particulate matter with diameter ≤ 2.5 μm (PM2.5). Annotated metabolites associated with exposure were then tested for relationships with the peripheral blood transcriptome using multivariate selection and network correlation. Week-averaged EC and OC levels, which were averaged across multiple shifts during the workweek, resulted in the greatest exposure-associated metabolic alterations compared to shift-averaged exposure levels. Metabolic changes associated with EC exposure suggest increased lipid peroxidation products, biomarkers of oxidative stress, thrombotic signaling lipids, and metabolites associated with endothelial dysfunction from altered nitric oxide metabolism, while OC exposures were associated with antioxidants, oxidative stress biomarkers and critical intermediates in nitric oxide production. Correlation with whole blood RNA gene expression provided additional evidence of changes in processes related to endothelial function, immune response, inflammation, and oxidative stress. We did not detect metabolic associations with PM2.5. This study provides an integrated molecular assessment of human exposure to traffic-related air pollutants that includes diesel exhaust. Metabolite and gene expression changes associated with exposure to EC and OC are consistent with increased risk of cardiovascular diseases and the adverse health effects of traffic-related air pollution.

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Acrolein-mediated changes in HUVEC miRNA

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