Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA106697 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cardiac and pulmonary responses to diesel engine particulate in Apo E(-/-) mice II
| PRJNA119015 | ENA
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
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.
2008-12-15 | GSE13160 | GEO
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
2009-10-30 | GSE17331 | GEO
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 and 5 days were subsequently analyzed by the 2-color microarray method. Keywords: stress response, disease state analysis
2008-06-30 | GSE11286 | GEO
Project description:In vivo endothelial transcriptomic responses to diesel engine exhaust are potentiated by hypercholesterolemia
| PRJNA109743 | ENA
Project description:Murine Pulmonary Responses to Ambient Baltimore Particulate Matter
| PRJNA103235 | ENA
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
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
Project description:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Keywords: wildtype vs Myc-null
2007-06-30 | GSE7162 | GEO