Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA391143 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The role of murine peroxisome proliferator-activated receptor-delta (PPARd) in mammary tumorigenesis was assessed. Microarrays were used to analyse global gene expression to determine changes in MMTV-PPARd transgenic mice versus wild-type mice and the effect of GW501516.
2013-05-31 | GSE34109 | GEO
Project description:Investigation of whole genome gene expression level changes in GW501516 (a Ppard ligand) or Il-4 treated Ppard-overexpressing RAW 264.7 macrophages as compared to vehicle. Alternative activation of adipose tissue resident macrophages inhibits obesity-induced metabolic inflammation. In the current study we profile genes regulated by two M2 inducers, Il-4 or Ppard agonists and find that alternative activation promotes the cell survival program, while inhibiting that of inflammation-related cell death.
2017-06-21 | GSE100237 | GEO
Project description:The role of murine peroxisome proliferator-activated receptor-delta (PPARd) in mammary tumorigenesis was assessed. Microarrays were used to analyse global gene expression to determine changes in MMTV-PPARd transgenic mice versus wild-type mice and the effect of GW501516. RNA was isolated (RNeasy Mini Kit, Qiagen) from mammary gland tissue of transgenic and wild-type mice maintained on normal rodent chow or 0.005% GW501516
2013-05-31 | E-GEOD-34109 | biostudies-arrayexpress
Project description:The PPAR (Peroxisome proliferator-activated receptor) family of nuclear receptors has three members: PPARg, PPARa and PPARd. Although they share similar structures, their biological functions are distinct. PPARg controls lipid storage and adipogenesis, while PPARd is associated with fat burning. The highly specific synthetic ligand for PPARd, GW501516, is a promising drug candidate for obesity and diabetes. Here we use Affymetrix microarray to analyze gene expression profile in mouse embryo fibroblasts treated with 100 nM GW501516 for 0, 2, 8 and 24 hours. These data may provide new clues into the molecular mechanism by which GW501516 ameliorates obesity and diabetes.
2013-12-31 | GSE20371 | GEO
Project description:The PPAR (Peroxisome proliferator-activated receptor) family of nuclear receptors has three members: PPARg, PPARa and PPARd. Although they share similar structures, their biological functions are distinct. PPARg controls lipid storage and adipogenesis, while PPARd is associated with fat burning. The highly specific synthetic ligand for PPARd, GW501516, is a promising drug candidate for obesity and diabetes. Here we use Affymetrix microarray to analyze gene expression profile in mouse embryo fibroblasts treated with 100 nM GW501516 for 0, 2, 8 and 24 hours. These data may provide new clues into the molecular mechanism by which GW501516 ameliorates obesity and diabetes. Wild type mouse embryonic fibroblasts (MEFs) stably infected with retroviruses MSCVpuro expressing PPARd were plated at 0.5 million per 10 cm dish. After overnight incubation, cells were treated with 100nM GW501516 for 0h, 2h, 8h and 48h. Cells were collected at subconfluent condition. Total RNAs were sequentially purified with Trizol (Invitrogen) and RNeasy kit (Qiagen) and analyzed in triplicate on Mouse Genome 430 2.0 Array (Affymetrix) at NIDDK Microarray Core Facility following standard protocols.
2013-12-31 | E-GEOD-20371 | biostudies-arrayexpress
Project description:Interventions: primary colorectal cancer group VS healthy control group:no intervention
Primary outcome(s): Peroxisome proliferator-activated receptor delta-87T>C
Study Design: Factorial
| 35322 | ecrin-mdr-crc
Project description:The role of peroxisome proliferator-activated receptor δ (PPARδ) activation on global gene expression and mitochondrial fuel utilization were investigated in human myotubes. Only 21 genes were up-regulated and 3 genes were down-regulated after activation by the PPARδ agonist GW501516. Pathway analysis showed up-regulated mitochondrial fatty acid oxidation, TCA cycle and cholesterol biosynthesis. GW501516 increased oleic acid oxidation and mitochondrial oxidative capacity by 2-fold. Glucose uptake and oxidation were reduced, but total substrate oxidation was not affected, indicating a fuel switch from glucose to fatty acid. Cholesterol biosynthesis was increased, but lipid biosynthesis and mitochondrial content were not affected. This study confirmed that the principal effect of PPARδ activation was to increase mitochondrial fatty acid oxidative capacity. Our results further suggest that PPARδ activation reduced glucose utilization through a switch in mitochondrial substrate preference by up-regulating pyruvate dehydrogenase kinase isozyme 4 and genes involved in lipid metabolism and fatty acid oxidation. Keywords: Expression profiling by array
2014-05-23 | GSE40789 | GEO
Project description:The formation of antigen-specific memory CD8+ T cells is one of the most important features of the adaptative immune system, allowing the establishment of long-term protection against secondary infections. Although emerging evidence suggests that metabolic reprogramming is crucial for memory T cell differentiation and survival, the underlying mechanisms that drive metabolic rewiring needed for memory T cells remain unclear. Here, we found that the nuclear receptor peroxisome proliferator-activated receptor-beta/delta (PPARβ/δ) was upregulated to instruct the metabolic reprogramming, including downregulation of aerobic glycolysis and the promotion of oxidative metabolism and fatty acid oxidation, that occurs during the transition toward the establishment of central memory CD8+ T cells. Mechanistically, the exposure to interleukin-15 (IL-15) and expression of T cell factor 1 (TCF1) could coordinately activated the PPARβ/δ pathway during acute viral infection and chronic antigen exposure contexts, counteracting apoptosis induced by antigen clearance and metabolic stress. Together, our work indicates that PPARβ/δ is a master metabolic regulator orchestrating the metabolic reprogramming required for the establishment of a metabolic profile favorable for T cells longevity.
2024-08-23 | GSE268419 | GEO
Project description:The formation of antigen-specific memory CD8+ T cells is one of the most important features of the adaptative immune system, allowing the establishment of long-term protection against secondary infections. Although emerging evidence suggests that metabolic reprogramming is crucial for memory T cell differentiation and survival, the underlying mechanisms that drive metabolic rewiring needed for memory T cells remain unclear. Here, we found that the nuclear receptor peroxisome proliferator-activated receptor-beta/delta (PPARβ/δ) was upregulated to instruct the metabolic reprogramming, including downregulation of aerobic glycolysis and the promotion of oxidative metabolism and fatty acid oxidation, that occurs during the transition toward the establishment of central memory CD8+ T cells. Mechanistically, the exposure to interleukin-15 (IL-15) and expression of T cell factor 1 (TCF1) could coordinately activated the PPARβ/δ pathway during acute viral infection and chronic antigen exposure contexts, counteracting apoptosis induced by antigen clearance and metabolic stress. Together, our work indicates that PPARβ/δ is a master metabolic regulator orchestrating the metabolic reprogramming required for the establishment of a metabolic profile favorable for T cells longevity.
2024-08-23 | GSE264017 | GEO
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