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Deregulation of PPAR-beta/delta target genes in tumor-associated macrophages by fatty acid ligands in the ovarian cancer microenvironment - RNAseq

ABSTRACT: Deregulation of PPAR-beta/delta target genes in tumor-associated macrophages by fatty acid ligands in the ovarian cancer microenvironment - RNAseq

PROVIDER: PRJEB7995 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR701467.fastq.gz	Fastqsanger.gz
	ERR701468.fastq.gz	Fastqsanger.gz
	ERR701469.fastq.gz	Fastqsanger.gz
	ERR701470.fastq.gz	Fastqsanger.gz
	ERR701471.fastq.gz	Fastqsanger.gz

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Similar Datasets

Deregulation of PPAR-beta/delta target genes in tumor-associated macrophages by fatty acid ligands in the ovarian cancer microenvironment - ChIPseq

Project description:Deregulation of PPAR-beta/delta target genes in tumor-associated macrophages by fatty acid ligands in the ovarian cancer microenvironment - ChIPseq

| PRJEB7994 | ENA

The roles of ppar-delta and ppar-gamma in regulating the metabolic switch between oxidation and storage of fats in white adipose tissue

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

The roles of ppar-delta and ppar-gamma in regulating the metabolic switch between oxidation and storage of fats in white adipose tissue

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

An in vitro effect of PPAR beta/delta ligands on transcriptomic profile of porcine corpus luteum during LPS-induced inflammation

Project description:The aim of this study was to determine the in vitro effects of peroxisome proliferator-activated receptor-beta/delta (PPARβ/δ) ligands on the transcriptomic profile of the LPS-stimulated pig CL in the mid-luteal phase of the estrous cycle using RNA-seq technology. The CL slices were incubated in the presence of LPS or in combination with LPS and the PPARβ/δ agonist-GW0724 (1 μmol/L or 10 μmol/L) or the antagonist-GSK3787 (25 μmol/L). We identified 117 differentially expressed genes after treatment with LPS; 102 and 97 differentially expressed genes after treatment respectively with the PPARβ/δ agonist at a concentration of 1 μmol/L or 10 μmol/L, as well as 88-after treatment with the PPARβ/δ antagonist

2022-09-01 | E-MTAB-12027 | biostudies-arrayexpress

Fasting upregulates the monocarboxylate transporter Mct1 at the rat blood-brain barrier through Ppar δ activation

Project description:Fasting is increasingly recognized as a potential therapeutic intervention in the field of neurology and psychiatry. However, its impact upon the blood-brain barrier (BBB), which strictly regulates the cerebral uptake of a wide range of endogenous compounds and drugs, is unknown. In this study we used a combination of in vivo and in vitro experiments to assess the response of the brain endothelium in rats that were fed ad libitum or fasted for one to three days. Fasting did not change the expression of the main drug efflux ATP-binding cassette transporters or P-glycoprotein activity at the BBB but modulated a restrictive set of solute carrier transporters. These included the monocarboxylate transporter Mct1, which is pivotal for the cerebral uptake of ketone bodies and thus for brain adaptation to fasting. Transcriptional profiling of freshly isolated brain endothelial cells showed that Ppar δ, a major lipid sensor, was selectively activated in response to fasting. In primary cultured rat brain endothelial cells, pharmacological agonists and free fatty acids selectively activated Ppar δ, resulting in the upregulation of Mct1 expression at the transcriptional and protein level. This was confirmed in vivo, by showing that dosing rats with a specific Ppar δ antagonist blocked the upregulation of Mct1 expression and activity induced by fasting. Altogether, our study describes for the first time a selective adaptive response of the brain vasculature to fasting and opens new perspectives for the metabolic manipulation of the BBB in the healthy or diseased brain.

2024-04-24 | GSE241803 | GEO

Transcriptomic profile of porcine corpus luteum after PPAR gamma ligands treatment

Project description:Transcriptomic profile of porcine corpus luteum after PPAR gamma ligands treatment

| PRJEB54775 | ENA

An in vitro effect of PPAR beta/delta ligands on transcriptomic profile of porcine corpus luteum during LPS-induced inflammation

Project description:An in vitro effect of PPAR beta/delta ligands on transcriptomic profile of porcine corpus luteum during LPS-induced inflammation

| PRJEB55168 | ENA

RNAi profiling by array of human WPMY-1 cells with PPARbeta/delta knock down and exposure to PPAR agaonists

Project description:Human WPMY-1 cells were depleted for PPARbeta/delta and exposed to the PPAR agonists GW501516.

2010-12-31 | E-MEXP-2756 | biostudies-arrayexpress

Real-time quantitative PCR analysis of fatty acid metabolism genes of liver tissue from wild-type and PPAR? (-/-) mice exposed to 2,4-dinitrotoluene (fatty acid)

Project description:2,4-dinitrotoluene (2,4-DNT), a nitroaromatic used in industrial and explosive manufacturing processes, is known to contaminate artillery ranges, demilitarization areas and munitions manufacturing facilities. Previous transcriptomic and lipidomic studies identified energy metabolism as a principle biochemical process affected by 2,4-DNT where up-stream effects on PPAR? signaling were hypothesized as themolecular initiating event for these effects. Here, the validity of this hypothetical adverse outcome pathway (AOP) was assessed by testing the hypothesis that 2,4-DNT-induced perturbations in PPAR? signaling and resultant downstream deficits in energy metabolism, especially from lipids, would result in organism-level impacts on exercise endurance. PPAR? knock-out (-/-) and wild-type (WT) mice were exposed for 14 days to vehicle or 2,4-DNT at a dose (134 mg/kg/day) that did not exhibit overt systemic toxicity. Mice performed an exercise challenge (forced swim) 1 day after the last dose. 2,4-DNT decreased swim times in WT and PPAR? (-/-) mice, but the effect was significantly less in PPAR? (-/-) mice indicating the critical of PPAR? in mediating 2,4-DNT-induced energy metabolism deficits. 2,4-DNT caused down-regulation of transcripts involved in fatty acid metabolism, gluconeogenesis, triacylglycerol catabolism, and the pentose phosphate pathway, and 2,4-DNT treated wild-type mice had decreased serum trigylcerides and increased serum glucose versus 2,4-DNT treated PPAR? (-/-) mice. Our results support the hypothesis that 2,4-DNT perturbs PPAR? signaling as a molecular initiating event therefore impacting energy metabolism, especially lipid metabolism, producing reduced exercise endurance in mice. RNA was isolated from liver tissue of vehicle or 2,4-DNT treated wild-type or PPAR? (-/-) mice (n=6) and RT-PCR performed to analyze genes involved in fatty acid metabolism

2014-06-30 | E-GEOD-50168 | biostudies-arrayexpress

Expression profiling of pancreatic beta-cells harboring a pancreatic-specific deletion of PPAR-beta

Project description:Peroxisome proliferator-activated receptor beta/delta protects against obesity by reducing dyslipidemia and insulin resistance via effects in various organs, including muscle, adipose tissue, liver, and heart. However, nothing is known about the function of PPAR-beta in pancreas, a prime organ in the control of glucose metabolism. To gain insight into so far hypothetical functions of this PPAR isotype in insulin production, we specifically ablated Ppar-beta in pancreas. The mutated mice developed a chronic hyperinsulinemia, due to an increase in both beta-cell mass and insulin secretion. Gene expression profiling indicated a broad repressive function of PPAR-beta impacting the vesicular compartment, actin cytoskeleton, and metabolism of glucose and fatty acids. Analyses of insulin release from the islets revealed an increased second-phase glucose-stimulated insulin secretion. Higher levels of PKD, PKC-delta and diacyglycerol in mutated animals lead to an enhanced formation of trans-Golgi network (TGN)-to-plasma-membrane transport carriers in concert with F-actin disassembly, which resulted in increased insulin secretion and its associated systemic effects. Taken together, these results provide evidence for PPAR-beta playing a repressive role on beta-cell growth and insulin exocytosis, which shed new light on its anti-obesity action.

2012-08-30 | GSE16048 | GEO

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