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Cardiac and pulmonary responses to diesel engine particulate in Apo E(-/-) mice

ABSTRACT: Mice deficient in Apolipoprotein E (Apoe E(-/-)) vs wild type mice were exposed to diesel engine particulate by single dose intratracheal instillation. The transcript-level response of the hearts after 24h and of the lungs after 24 h and 5 days were subsequently analyzed by the 2-color microarray method. Keywords: stress response, disease state analysis

ORGANISM(S): Mus musculus

PROVIDER: GSE11286 | GEO | 2008/06/30

SECONDARY ACCESSION(S): PRJNA106697

REPOSITORIES: GEO

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Cardiac and pulmonary responses to diesel engine particulate in Apo E(-/-) mice II

Project description:Mice deficient in Apolipoprotein E (Apoe E(-/-)) vs wild type mice were exposed to diesel engine particulate by single dose intratracheal instillation. The transcript-level response of the hearts after 24h and of the lungs after 24 h were subsequently analyzed by the 2-color microarray method. Keywords: stress response, disease state analysis Three mice of the Apo E (-/-) strain were exposed to diesel engine particulate from the National Institute of Standards and Technology via intratracheal instillation. Controls consisted of 3 littermates exposed to saline vehicle. Similarly, three wild type mice were similarly exposed to diesel particulate and three to vehicle control. 24 hours after exposure, mice were humanely sacrificed by carbon dioxide asphyxiation and the hearts and lungs were collected and frozen for analysis of total RNA. In each biological replicate, 2 color microarrays were utilized to compare pooled RNA representing all three animals of each strain, and in each condition and in each tissue; each biological replicate was performed with a dye reversal. Biological replicates of the wild type mice responses to diesel engine particulate were performed three times for heart and lung.

2010-06-23 | E-GEOD-17331 | biostudies-arrayexpress

Cardiac and pulmonary responses to diesel engine particulate in Apo E(-/-) mice II

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In vivo endothelial transcriptomic responses to diesel engine exhaust are potentiated by hypercholesterolemia

Project description:By means of Operon V3 microarrrays, the in vivo, aortic endothelial transcriptomic responses to chronic (30 day) whole body exposure to diesel exhaust were assessed in wild type and Apo E (-/-) mice. The in vitro response of cultured Svec 4-10 cells exposed to a soluble extract extract of diesel engine particulate were similarly assessed.

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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.

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Lung cell responses to ship diesel exhaust particles

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

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

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Proteome-wide changes in primary skin keratinocytes exposed to diesel particulate extract – a role for antioxidants in skin health

Project description:Environmental air pollution such as diesel smoke emission has been shown to have an adverse effect on human skin. Although epidemiological studies showing adverse effects such as oxidative stress-induced aging exists, studies showing the cellular and molecular response to such stress are rare. Using a primary skin keratinocyte model and TMT-based quantitative proteomics strategy, we studied the effects of chronic exposure to diesel particulate matter (DPE) and DPE vapor on the cellular proteome and the ability of a known anti-oxidant Vitamin E in ameliorating such changes. LC-MS3 analysis of DPE and/or its vapor exposed skin keratinocytes resulted in quantification of 4,490 proteins of which 201 and 374 proteins were significantly dysregulated (≥1.5 fold, p-value ≥0.05) in each condition, respectively. We observed distinct molecular alterations in chronic DPE and DPE vapor exposure models. Dysregulation of several cellular processes such as cell cycle and gene regulation, oxidative stress response proteins, skin barrier integrity and skin hydration were observed in both DPE and DPE vapor exposed cells.

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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.

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Lung cell responses to ship diesel exhaust particles

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2015-02-01 | E-GEOD-63962 | biostudies-arrayexpress

Differential Transcriptional Changes in Mice Exposed to Chemically Distinct Diesel Samples

Project description:Epidemiological studies have linked exposure to ambient particulate matter (PM) with increased asthmatic symptoms. Diesel exhaust particles (DEP) are a predominant source of vehicle derived ambient PM, and experimental studies have demonstrated that they may have adjuvant potential when given with an antigen. We previously compared 3 DEP samples: N-DEP, A-DEP, and C-DEP in a murine ovalbumin (OVA) mucosal sensitization model and reported the adjuvant activity to be: C-DEP ? A-DEP > N-DEP. The present study analyzed gene expression changes from the lungs of these mice. Transcription profiling demonstrated that all the DEP samples altered cytokine and toll-like receptor pathways regardless of type, with or without antigen sensitization. Further analysis of DEP exposure with OVA showed that all DEP treatments altered networks involved in immune and inflammatory responses. The A- and C-DEP/OVA treatments induced differential expression of apoptosis pathways in association with stronger adjuvant responses, while expression of cell cycle control and DNA damage pathways were also altered in the C-DEP/OVA treatment. This comprehensive approach using gene expression analysis to examine changes at a pathway level provides detailed information on events occurring in the lung after DEP exposure, and confirms that the most bioactive sample induced many more individual genes and changes in immuno-regulatory and homeostatic pathways. Female BALB/C mice (8-10 weeks old) were randomly divided into 8 treatment groups containing 3 mice each and exposed to saline, 20 ug ovalbumin, 150 ug diesel exhaust particles (either C-DEP, A-DEP, or N-DEP), or diesel exhaust particles + ovalbumin by intranasal instillation on Days 0 and 13 and necropsied 18 hrs latter.

2010-07-10 | E-GEOD-22357 | biostudies-arrayexpress

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