Effect PPARb/d knockout in white adipose tissue
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE8344 | GEO | 2007/07/04
SECONDARY ACCESSION(S): PRJNA101351
REPOSITORIES: GEO
Similar Datasets
Project description:Analysis of white adipose tissue of PPARb/d knockout mice. Data may point towards putative target genes of PPARb/d and thus the function of PPARb/d in white adipose tissue. Datasets were used to identify glycogen synthase 2 as novel PPAR target. Experiment Overall Design: Three month old male PPARb/d knock-out mice were on a mixed background (Sv129/C57BL/6). Wild-type littermates served as control animals. Animals received standard chow. Epididymal white adipose tissue (WAT) was removed and total RNA was isolated and pooled afterwards (five animals per group). Pooled RNA was hybridized to Affymetrix mouse genome 430 2.0 arrays arrays. Five microgram total RNA was labeled according to the ENZO-protocol, fragmented and hybridized according to Affymetrix protocols.
2008-06-16 | E-GEOD-8344 | biostudies-arrayexpress
Project description:The role of PPARβ/δ in maintaining skin homeostasis during skin injury or inflammation has been widely studied. However, the majority of these reports based their studies in PPARβ/δ found in keratinocytes, which is the major cell type of the skin epidermis. The skin is mainy made up of the epidermis and dermis, and skin homeostasis is tightly regulated by complex crosstalks between epidermis and dermis. The dermis is predominantly made up of fibroblasts, and the predominant PPAR subtype in dermal fibroblasts is PPARβ/δ. Knowledge in the role of fibroblasts PPARβ/δ in skin homeostasis is lacking. To identify gene changes leading to phenotypical and biological functions alterations upon deletion of fibroblasts PPARβ/δ, we performed a comparative microarray gene expression analysis between Pparb/d^fl/fl and FSPCre-Pparb/d^fl/fl mice.
2018-04-03 | GSE71419 | GEO
Project description:Stroma secretes complex regulatory signals, including reactive oxygen species, that are involved in mediating cancer development. Ablation of PPARB expression in fibroblastic cells results in modulation of oxidative stress signals that lead By means of gene expression analysis, we seek to identify key gene expression changes in tumor epithelial cells between FSPCre-PPARB -/- and PPARB flox/flox mice.
2018-08-05 | GSE97339 | GEO
Project description:Stroma secretes a multitude of regulatory signals that are involved in mediating intestinal development. Ablation of PPARB expression in fibroblastic cells results in modulation of oxidative stress signals that lead to altered intestinal morphology and gene expression profiles Through gene chip expression profiling, we seek to identify key changes in intestinal mucosal gene expression profiling between FSPCre-PPARB flox/flox and PPARB flox/flox mice.
2018-08-05 | GSE97472 | GEO
Project description:Beneficial effects have been reported in individuals undergoing fasting to treat excessive weight gain and obesity. To better understand the effects of starvation on the transcriptome and lipid metabolism of white adipose tissue, we established a mouse model of 24-hour fasting using wild type C57BL/6J mice, and performed RNA-seq analysis of the white adipose tissue from the epididymis of fasted mice and control mice. Compared with the control fed mice, these fasted mice showed suppressed lipid synthesis and inhibited insulin signaling, while the lipolysis and gluconeogenesis were enhanced to maintain blood sugar stability. Specifically, the fasted mice had reduced volume of adipose tissues, increased levels of serum NEFA and ANP. In epididymal white adipose tissue, starvation increased the NEFA content, up-regulated the mRNA levels of Atgl, Adrb2, Anp, and Npr1, and promoted the phosphorylation of Hsl. Notably, bioinformatics analysis of the RNA-seq data showed that 24-hour fasting-induced alterations in lipid metabolism was associated with suppressed AMPK signaling and enhanced PPAR signaling in white adipose tissue, which was verified by quantitative PCR. Collectively, these findings supported that starvation promoted the conversion of energy-supplying substrates from glucose to fat. Our work sheds new light on harnessing the plasticity of adipose tissues and the AMPK/PPAR signaling pathways to develop potential strategies to combat obesity and other glucose/lipid metabolisms-associated human diseases.
2022-10-01 | GSE207913 | GEO
Project description:Obesity is a major risk factor for the development of insulin resistance and type II diabetes. The nuclear receptors PPAR delta and PPAR gamma play a central role in regulating metabolism in adipose tissue, as well as being targets for the treatment of insulin resistance. The metabolic effects of PPAR delta and PPAR gamma activation have been examined both in vivo in white adipose tissue from ob/ob mice and in vitro in cultured 3T3-L1 adipocytes using a combined 1H NMR spectroscopy and mass spectrometry metabolomic methodology to understand the contrasting roles of these receptors. These steady state measurements were supplemented with 13C-stable isotope substrate labeling to assess fluxes, respirometry and transcriptomic microarray analysis. The metabolic effects of the two receptors were readily distinguished, with PPAR gamma ?activation characterised by increased fat storage and fat synthesis/elongation, while activation of PPAR delta caused increased fatty acid beta-oxidation, TCA cycle rate and oxidation of extracellular branch chain amino acids. Stimulated glycolysis and increased desaturation of fatty acids were the only common pathways. PPAR delta has a role as an anti-obesity target as well as an anti-diabetic. Total RNA obtained from cultured 3T3-L1 cells treated for 48 hours with either DMSO control, GW610742 PPARd agonist or GW347845 PPARg agonist and compared.
2011-07-13 | E-GEOD-26207 | biostudies-arrayexpress
Project description:Obesity is a major risk factor for the development of insulin resistance and type II diabetes. The nuclear receptors PPAR-delta and PPAR-gamma play a central role in regulating metabolism in adipose tissue, as well as being targets for the treatment of insulin resistance. The metabolic effects of PPAR-delta and PPAR-gamma activation have been examined both in vivo in white adipose tissue from ob/ob mice and in vitro in cultured 3T3-L1 adipocytes using a combined 1H NMR spectroscopy and mass spectrometry metabolomic methodology to understand the contrasting roles of these receptors. These steady state measurements were supplemented with 13C-stable isotope substrate labeling to assess fluxes, respirometry and transcriptomic microarray analysis. The metabolic effects of the two receptors were readily distinguished, with PPAR-gamma activation characterised by increased fat storage and fat synthesis/elongation, while activation of PPAR-delta caused increased fatty acid beta-oxidation, TCA cycle rate and oxidation of extracellular branch chain amino acids. Stimulated glycolysis and increased desaturation of fatty acids were the only common pathways. PPAR-delta has a role as an anti-obesity target as well as an anti-diabetic.
2011-07-14 | GSE26207 | GEO
Project description:Solar radiation is the major source of human exposure to UV radiation, the major carcinogen in skin cancers, by triggering a number of cellular responses that can indirectly or directly induce DNA damage. Skin cells attempt to repair these damages by activating cascades of DNA Damage Response mechanisms to safeguard genome integrity, thereby preventing skin cancers. The role of PPARb - a druggable transcription factor, in the development of UV-dependent skin cancers is not mechanistically elucidated. We have shown previously that PPARb knockout mice are less prone to UV-induced skin cancers. Here, we report on our global transcriptomic analysis revealing that PPARb directly regulates gene expression programs associated with cell cycle and DNA repair pathways in normal human epidermal keratinocytes. We show that in these cells, as well as in malignant human keratinocytes and in human melanoma cells, PPARb controls cellular proliferation and cell cycle progression and its depletion leads to cell cycle arrest. We also show that PPARb controls the response of normal human epidermal keratinocytes to UV-induced DNA damage. PPARb depletion decreases the expression and/or activation of multiple effectors of DNA Damage Response (DDR) pathway and favours the apoptotic response of human keratinocytes to UV irradiation. Our preclinical data of a PDX melanoma model demonstrated that the depletion or inhibition of PPARb delays of blocks tumor formation. Our data suggest that PPARb inhibition can be considered as a therapeutic target for the prevention of UV-induced skin cancers in vulnerable population, by attenuating the DDR and eliminating skin cells with high UV-induced mutational burden.
2024-12-18 | GSE263846 | GEO
Project description:The aim of this study was to identify genes expressed selectively in brown adipose tissue as compared to white adipose tissue from the same animals. This analysis provides a gene set that is brown and white adipose selective. Keywords: tissue comparison from mice
2007-06-08 | GSE8044 | GEO