Project description:The PPARD ligand response (agonist and inverse agonist) in monocyte derived macrophages from 3 healthy donors was assesed via RNAseq.
Project description:Transcriptome profiles for innate and adaptive immune stimuli important for host response against mycobacteria. Human monocyte-derived macrophages were stimulated with TLR2/1 ligand and interferon-g, stimuli present during innate and adaptive immune responses, respectively.
Project description:Circadian biology regulates inflammatory responses in mice via the clock protein REVERBα, resulting in altered mortality and morbidity. The influence of this immune-modulation pathway in humans is unclear, but may affect outcomes after transplant. We sought to determine whether the circadian clock affects primary graft dysfunction after lung transplantation, and the role of the clock protein REVERBα. In this study we investigated the action of a synthetic REVERB ligand, (GSK4112) in human monocyte-derived macrophages.
Project description:Primary mouse macrophages from wt and PPARD-/- mice, elucidated with thioglycollate, were exposed to PPARbeta/delta specific ligands and the resulting changes in global gene expression were measured.
Project description:Recently the role of PPARβ/δ in angiogenesis has been revealed, and we hypothesized that the crosstalk between hypoxia and PPARβ/δ on endothelial cells may exsist. To elucidate the interaction between two signalings, we report the comprehensive change of transcripts induced by PPARβ/δ agonist (GW501516) and/or hypoxia. We used microarray analysis of HUVECs treated with PPARβ/δ agonist (GW501516) and/or hypoxia (1% O2) for 24-hours, and we identified a group of consistently up- or down-regulated genes.
Project description:H3K27Ac is one of the expressed enhancer markers, PPARβ/δ is a transcription factor and Pol II (RNA polymerase II) is an enzyme which catalyzes the transcription of DNA to synthesize precursors of mRNA and most snRNA and microRNA. These genomic localization in endothelial cells is unknown in endothelial cells. This time, we established a new antibody for H3K27ac, PPARβ/δ and Pol II and performed ChIP-seq to identify H3K27ac, PPARβ/δ and Pol II binding site in whole genome manner under PPARβ/δ agonist and/or hypoxia.
Project description:H3K27Ac is one of the expressed enhancer markers, PPARβ/δ is a transcription factor and Pol II (RNA polymerase II) is an enzyme which catalyzes the transcription of DNA to synthesize precursors of mRNA and most snRNA and microRNA. These genomic localization in endothelial cells is unknown in endothelial cells. This time, we established a new antibody for H3K27ac, PPARβ/δ and Pol II and performed ChIP-seq to identify H3K27ac, PPARβ/δ and Pol II binding site in whole genome manner under PPARβ/δ agonist and/or hypoxia. We used chromatin immunoprecipitation with deep sequencing (ChIP-seq) of HUVECs treated with PPARβ/δ agonist (GW501516 100nM) and/or hypoxia (1%O2) for 24hours, then H3K27ac, PPARβ/δ and Pol II binding regions were identified. Normoxia and DMSO was used as a control condition. HUVECs were used within the first 6 passages.
Project description:Recently the role of PPARβ/δ in angiogenesis has been revealed, and we hypothesized that the crosstalk between hypoxia and PPARβ/δ on endothelial cells may exsist. To elucidate the interaction between two signalings, we report the comprehensive change of transcripts induced by PPARβ/δ agonist (GW501516) and/or hypoxia. We used microarray analysis of HUVECs treated with PPARβ/δ agonist (GW501516) and/or hypoxia (1% O2) for 24-hours, and we identified a group of consistently up- or down-regulated genes. HUVECs were used within the first 6 passages. HUVECs were treated with PPARβ/δ agonist (GW501516) at a concentration of 100 nM and/or hypoxia (1% O2) for 24-hours. Same concentration of DMSO was used as a control sample, and as to the oxgen, normoxia was used as a control condition.
