Meta-analysis of primary target genes of peroxisome proliferator-activated receptors

A combined experimental and in silico approach identifies Peroxisome Proliferator Activated Receptor (PPAR) binding sites and six novel target genes in the human genome

Photocatalytic Decomposition of Formic Acid on Mo2C-Containing Catalyst

Soluble components in the peripheral blood from experimental exposure of 14 healthy subjects to filtered air and wood smoke. Samples were collected before (pre), at 24 h and 44 h after exposure, to air and wood smoke. Data are given as medians with interquartile range. (DOCX 62 kb

Emissions from a modern log wood masonry heater and wood pellet boiler : Composition and biological impact on air-liquid interface exposed human lung cancer cells

The consumption of wood fuel is markedly increasing in developing and industrialized countries. Known side effects of wood smoke inhalation manifest in proinflammatory signaling, oxidative stress, DNA damage and hence increased cancer risk. In this study, the composition and acute biological impact of emissions of state-of-the-art wood combustion compliances: masonry heater (MH) and pellet boiler (PB) were investigated. Therefore A549 cells were exposed to emission aerosols in an automated air-liquid interface exposure station followed by cytotoxicity, transcriptome and proteome analyses. In parallel, aerosols were subjected to a chemical and physical haracterization. Compared to PB, the MH combustion at the same dilution ratio resulted in a 3-fold higher particle mass concentration (PM2.5) and deposited dose (PB: 27 $\pm$ 2 ng/cm2, MH; 73 $\pm$ 12 ng/cm2). Additionally, the MH aerosol displayed a substantially larger concentration of aldehydes, polycyclic aromatic hydrocarbons (PAH) or oxidized PAH. Gene ontology analysis of transcriptome of A549 cells exposed to MH emissions revealed the activation of proinflammatory response and key signaling cascades MAP kinase and JAK-STAT. Furthermore, CYP1A1, an essential enzyme in PAH metabolism, was induced. PB combustion aerosol activated the proinflammatory marker IL6 and different transport processes. The proteomics data uncovered induction of DNA damage-associated proteins in response to PB and DNA doublestrand break processing proteins in response to MH emissions. Taking together, the MH produces emissions with a higher particle dose and more toxic compounds while causing only mild biological responses. This finding points to a significant mitigating effect of antioxidative compounds in MH wood smoke

Extra-genomic functionality of the PPRE-containing promoter regions of PPAR target genes

Reporter gene assays were performed with extracts from HEK293 and HepG2 cells that were transiently transfected with reporter constructs containing genomic regions of eight human PPAR target genes (please note that the gene forms a cluster with the genes and ). These were co-transfected with empty expression vector (endogenous PPAR) or the indicated expression vectors for PPARα, PPARγ and PPARβ/δ. Cells were then treated for 16 h with solvent or PPAR subtype-specific ligands. Relative luciferase activity was determined and normalized to the activity of empty cloning vector control co-transfected with empty expression vector (dashed horizontal red line). The genomic regions were subdivided according to their location into close to TSS (a, d), upstream of TSS (b, e) and downstream of TSS (c, f); for further details see Figure 3 and Table 2. Columns represent the means of at least three experiments and bars indicate standard deviations. Two-tailed Student's -tests were performed to determine the significance of the ligand induction in reference to solvent controls (*< 0.05, **< 0.01, ***< 0.001).<p><b>Copyright information:</b></p><p>Taken from "Meta-analysis of primary target genes of peroxisome proliferator-activated receptors"</p><p>http://genomebiology.com/2007/8/7/R147</p><p>Genome Biology 2007;8(7):R147-R147.</p><p>Published online 25 Jul 2007</p><p>PMCID:PMC2323243.</p><p></p

SOM analysis of established primary PPAR target genes, clusters III and IV

The genes were sorted by SOM analysis with respect to overall PPRE pattern similarity and their evolutionary conservation into cluster III and cluster IV. For more details, see the Figure 6 legend.<p><b>Copyright information:</b></p><p>Taken from "Meta-analysis of primary target genes of peroxisome proliferator-activated receptors"</p><p>http://genomebiology.com/2007/8/7/R147</p><p>Genome Biology 2007;8(7):R147-R147.</p><p>Published online 25 Jul 2007</p><p>PMCID:PMC2323243.</p><p></p