Similar Datasets
Project description:PPAR-y agonists promote the resolution of myelofibrosis in preclinical models
| PRJNA593237 | ENA
Project description:Transcriptional consequences of pharmacologic PPAR a, d, & g agonist administration in murine liver, heart, kidney, and skeletal muscle
2015-08-31 | GSE27948 | GEO
Project description: Not available
| S-EPMC8159700 | biostudies-literature
Project description: Not available
| S-EPMC3664607 | biostudies-literature
Project description:Lipid metabolism is essential in maintaining energy homeostasis in multicellular organisms. In vertebrates, the peroxisome proliferator-activated receptors (PPARs, NR1C) regulate the expression of many genes involved in these processes. Four Ppar subtypes from Atlantic cod (Gadus morhua) were recently cloned and characterized. However, the downstream regulatory role of Ppars in cod lipid metabolism is presently not well understood or described. Here we study the involvement of Atlantic cod Ppar subtypes in systemic regulation of lipid metabolism using the model agonists WY14,643, GW501516, and tetradecylthioacetic acid, employing a multiple omics approach after an in vivo exposure situation.
2022-09-20 | PXD031739 | Pride
Project description:We examined the alternation of gene expression by MCC-555, rosiglitazone (RGZ) and 15-deoxy-Δ12, 14-prostaglandin J2 (PGJ2) in human colorectal adenocarcinoma HCT-116 cells. Keywords: effects of PPAR-gamma agonists
2008-06-10 | GSE9183 | GEO
Project description:Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that act as ligand-activated transcription factors. Although prescribed for dyslipidemia and type-II diabetes, PPAR agonists have demonstrated therapeutic properties for several brain disorders, including alcohol dependence. PPAR agonists decrease ethanol consumption and reduce withdrawal severity and susceptibility to stress-induced relapse in rodents. However, the cellular and molecular mechanisms facilitating these properties have yet to be investigated and little is known about their effects in the brain. We tested three PPAR agonists in a continuous access two-bottle choice (2BC) drinking paradigm and found that tesaglitazar and fenofibrate decreased ethanol consumption in male C57BL/6J mice while bezafibrate did not. Hypothesizing that fenofibrate and tesaglitazar are causing brain gene expression changes that precipitate the reduction in ethanol drinking, we gave daily oral injections of fenofibrate, tesaglitazar and bezafibrate to mice for eight consecutive days and collected liver, prefrontal cortex and amygdala 24 hours after last injection. RNA was isolated and purified using MagMAX-96 Total RNA Isolation Kit. Biotinylated, amplified cRNA was generated using Illumina TotalPrep RNA Amplification Kit and hybridized to Illumina MouseWG-6 v2.0 Expression microarrays.
2015-04-14 | GSE67796 | GEO
Project description:Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that act as ligand-activated transcription factors. Although prescribed for dyslipidemia and type-II diabetes, PPAR agonists have demonstrated therapeutic properties for several brain disorders, including alcohol dependence. PPAR agonists decrease ethanol consumption and reduce withdrawal severity and susceptibility to stress-induced relapse in rodents. However, the cellular and molecular mechanisms facilitating these properties have yet to be investigated and little is known about their effects in the brain. We tested three PPAR agonists in a continuous access two-bottle choice (2BC) drinking paradigm and found that tesaglitazar and fenofibrate decreased ethanol consumption in male C57BL/6J mice while bezafibrate did not. Hypothesizing that fenofibrate and tesaglitazar are causing brain gene expression changes that precipitate the reduction in ethanol drinking, we gave daily oral injections of fenofibrate, tesaglitazar and bezafibrate to mice for eight consecutive days and collected liver, prefrontal cortex and amygdala 24 hours after last injection. RNA was isolated and purified using MagMAX-96 Total RNA Isolation Kit. Biotinylated, amplified cRNA was generated using Illumina TotalPrep RNA Amplification Kit and hybridized to Illumina MouseWG-6 v2.0 Expression microarrays. Mice were divided into four groups (N=10 per group): fenofibrate, tesaglitazar, bezafibrate and saline. See summary and protocols for details.
2015-04-14 | E-GEOD-67796 | biostudies-arrayexpress
Project description:Aims: To compare the molecular and biologic signatures of a balanced dual peroxisome proliferator-activated receptor-α/γ (PPAR-α/γ) agonist, aleglitazar, with tesaglitazar (a dual PPAR-α/γ agonist) or combination of pioglitazone (PPAR-γ agonist)/fenofibric acid (PPAR-α agonist) in human hepatocytes. Methods and Results: Gene expression microarray profiles were obtained from primary human hepatocytes treated with EC50-aligned low, medium, and high concentrations of the three treatments. A systems-biology approach, Causal Network Modeling, was used to model the data to infer upstream molecular mechanisms that may explain the observed changes in gene expression. Aleglitazar, tesaglitazar and pioglitazone/fenofibric acid, each induced unique transcriptional signatures, despite comparable core PPAR signaling. Although all treatments inferred qualitatively similar PPAR-α signaling, aleglitazar was inferred to have greater effects on high- and low-density lipoprotein cholesterol levels than tesaglitazar and pioglitazone/fenofibric acid, due to greater number of gene expression changes in pathways related to HDL and LDL metabolism. Distinct transcriptional and biologic signatures were also inferred for stress responses, which appeared to be less affected by aleglitazar than the comparators. In particular, pioglitazone/fenofibric acid was inferred to increase NFE2L2 activity, a key component of the stress response pathway, while aleglitazar had no significant effect. All treatments were inferred to decrease proliferative signaling. Conclusions: Aleglitazar induces transcriptional signatures related to lipid parameters and stress responses that are unique from other dual PPAR-α/γ treatments. This may underlie observed favorable changes in lipid profiles in animal and clinical studies with aleglitazar and suggests a differentiated gene profile compared with other dual PPAR-α/γ agonist treatments.
2011-10-22 | GSE33152 | GEO
Project description:Pharmacological activation of the transcription factor PPAR gamma lowers blood pressure and improves glucose tolerance in humans. In contrast, naturally occurring mutations (e.g., P467L, V290M) in the ligand binding domain of PPAR gamma in humans leads to severe insulin resistance and early-onset hypertension. Experimental evidence, including whole genome expression profiling, suggests that these mutant versions of PPAR gamma act in a dominant negative manner. Because PPAR gamma is expressed in a variety of cell types and tissues, we generated a transgenic mouse model (SP467L) specifically targeting dominant negative PPAR gamma to the vascular smooth muscle cells in order to determine the action of PPAR gamma in the blood vessel independent of its systemic metabolic actions. In the data set provided herein, we examined the gene expression profile in mesenteric vessels from SP467L mice and their control littermates using the Affymetrix mouse exon 1.0 ST array.
2012-09-24 | GSE36482 | GEO