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

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

PROVIDER: PRJEB7994 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR701453.fastq.gz	Fastqsanger.gz
	ERR701455.fastq.gz	Fastqsanger.gz
	ERR701458.fastq.gz	Fastqsanger.gz
	ERR701460.fastq.gz	Fastqsanger.gz

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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

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

| PRJEB7995 | ENA

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

Deregulation of PPARβ/δ target genes in tumor-associated macrophages by fatty acid ligands in the ovarian cancer microenvironment - ChIPseq

Project description:PPARD and RXR genome wide binding in tumor associated macrophages from serous ovarian carcinoma was characterized.

2015-06-01 | E-MTAB-3166 | biostudies-arrayexpress

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

Project description:The transcriptome of serous ovarian cancer tumor associated macrophages was characterized. Additionally, their transcription response to PPARD agonists and inverse agonists in cell culture was analyzed.

2015-05-31 | E-MTAB-3167 | biostudies-arrayexpress

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

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

Deregulation of PPARβ/δ target genes in tumor-associated macrophages by fatty acid ligands in the ovarian cancer microenvironment.

Project description:The nuclear receptor peroxisome proliferator-activated receptor β/δ (PPARβ/δ) is a lipid ligand-inducible transcription factor associated with macrophage polarization. However, its function in tumor-associated macrophages (TAMs) has not been investigated to date. Here, we report the PPARβ/δ-regulated transcriptome and cistrome for TAMs from ovarian carcinoma patients. Comparison with monocyte-derived macrophages shows that the vast majority of direct PPARβ/δ target genes are upregulated in TAMs and largely refractory to synthetic agonists, but repressible by inverse agonists. Besides genes with metabolic functions, these include cell type-selective genes associated with immune regulation and tumor progression, e.g., LRP5, CD300A, MAP3K8 and ANGPTL4. This deregulation is not due to increased expression of PPARβ/δ or its enhanced recruitment to target genes. Instead, lipidomic analysis of malignancy-associated ascites revealed high concentrations of polyunsaturated fatty acids, in particular linoleic acid, acting as potent PPARβ/δ agonists in macrophages. These fatty acid ligands accumulate in lipid droplets in TAMs, thereby providing a reservoir of PPARβ/δ ligands. These observations suggest that the deregulation of PPARβ/δ target genes by ligands of the tumor microenvironment contributes to the pro-tumorigenic polarization of ovarian carcinoma TAMs. This conclusion is supported by the association of high ANGPTL4 expression with a shorter relapse-free survival in serous ovarian carcinoma.

| S-EPMC4537024 | biostudies-literature

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

chipseq

Project description:chipseq data

| PRJEB39779 | ENA

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

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