Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparative gene expression profile of PPARg and RARa ligand treated human dendritic cells

ABSTRACT: Our data indicated that activation of the PPARg nuclear receptor induces a retinoid response in human dendritic cells. In order to assess the contribution of retinoid signaling to the PPARg response we decided to use a combination of pharmacological activators and inhibitors of these pathways. Cells were treated with the synthetic PPARg ligand rosiglitazone (RSG), or with RSG along with the RARa antagonist (AGN193109) to block RARa mediated gene expression, or the RARa specific agonists (AM580) alone. This design allows one to determine if retinoid signaling is a downstream event of PPARg activation and what portion of PPARg regulated genes are regulated via induced retinoid signaling. Keywords: ligand response

ORGANISM(S): Homo sapiens

PROVIDER: GSE5679 | GEO | 2006/09/19

SECONDARY ACCESSION(S): PRJNA96965

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcription profiling of human freshly isolated PPARg and RARa ligand treated dendritic cells

Project description:Our data indicated that activation of the PPARg nuclear receptor induces a retinoid response in human dendritic cells. In order to assess the contribution of retinoid signaling to the PPARg response we decided to use a combination of pharmacological activators and inhibitors of these pathways. Cells were treated with the synthetic PPARg ligand rosiglitazone (RSG), or with RSG along with the RARa antagonist (AGN193109) to block RARa mediated gene expression, or the RARa specific agonists (AM580) alone. This design allows one to determine if retinoid signaling is a downstream event of PPARg activation and what portion of PPARg regulated genes are regulated via induced retinoid signaling. Experiment Overall Design: Monocytes were cultured for 5 days with 500 U/ml IL-4 and 800 U/ml GM-CSF, cytokine treatment was repeated at day 3. Ligands were added at the beginning of differentiation but AGN193109 (AGN) treatment was repeated at day 3. Cells were obtained from three healthy individuals (three biological replicates) and cells were treated with vehicle (DC), 2.5 uM rosiglitazone (DC RSG), 100 nM AM580 (DC AM). RSG treatment was also combined with 1 uM AGN193109 (DC RSG AGN) in this case two biological replicates was used (RNA was obtained from 2. and 3. individuals).

2009-04-25 | E-GEOD-5679 | biostudies-arrayexpress

PPARg regulated gene expression in human dendritic cells

2007-08-20 | GSE8658 | GEO

PPARg and IL-4-induced gene expression data from PPARg +/- LysCre and PPARg fl/- LysCre mouse bone marrow-derived macrophages

Project description:Conditional macrophage-specific PPARg knockout mice were generated on C57Bl/6 background by breeding PPARg fl/- (one allele is floxed, the other is null) and lysozyme Cre transgenic mice. PPARg and IL-4 signaling was analyzed on bone marrow-derived macrophages. Bone marrow of 3 mice per group was isolated and differentiated to macrophages with M-CSF (20 ng/ml). 20 ng/ml IL-4 was used to induce alternative macrophage activation and 1 uM Rosiglitazone (RSG) was used to activate PPARg. From each mouse 4 samples were generated: 1. M-CSF, 2. M-CSF+RSG, 3. IL-4 and 4. IL-4+RSG. All compounds were added throughout the whole differentiation process, and fresh media was added every other day. Control cells were treated with vehicle (DMSO:ethanol). After 10 days, RNA was isolated and gene expression profiles were analyzed using Mouse Genome 430 2.0 microarrays from Affymetrix. 3 PPARg +/- LysCre and 3 PPARg fl/- LysCre mice were used to isolate bone marrow and from each macrophages were differentiated with or without IL-4 and simultaneously treated with vehicle or RSG. Altogether we analyzed 24 samples with 3 biological replicates as below.

2010-11-18 | E-GEOD-25123 | biostudies-arrayexpress

PPARg and IL-4-induced gene expression data from PPARg +/- LysCre and PPARg fl/- LysCre mouse bone marrow-derived macrophages

2010-11-18 | GSE25123 | GEO

PPARg and IL-4-induced gene expression data from PPARg +/- LysCre and PPARg fl/- LysCre mouse bone marrow-derived alternatively activated macrophages and immature dendritic cells (iDCs)

Project description:Conditional macrophage-specific PPARg knockout mice were generated on C57Bl/6 background by breeding PPARg fl/- (one allele is floxed, the other is null) and lysozyme Cre transgenic mice. PPARg and IL-4 signaling was analyzed on bone marrow-derived macrophages. Bone marrow of 4 mice per group was isolated and differentiated to alternatively activated macrophages with 20 ng/ml M-CSF and 20 ng/ml IL-4 or to iDCs with 20 ng/ml GM-CSF+20 ng/ml IL-4. 1 uM Rosiglitazone (RSG) was used to activate PPARg. From each mouse 4 samples were generated: 1. M-CSF+IL-4, 2. M-CSF+IL-4+RSG, 3. GM-CSF+IL-4 and 4. GM-CSF+IL-4+RSG. All compounds were added throughout the whole differentiation process, and fresh media was added every other day. Control cells were treated with vehicle (DMSO:ethanol). After 9 days, RNA was isolated and gene expression profiles were analyzed using ABI Mouse Genome Survey Arrays. 4 PPARg +/- LysCre and 4 PPARg fl/- LysCre mice were used to isolate bone marrow and from each alternatively activated macrophages were differentiated with IL-4 and simultaneously treated with vehicle or RSG, iDCs were differentiated with GM-CSF+IL-4 and simultaneously treated with vehicle or RSG. Altogether we analyzed 32 samples with 4 biological replicates as below.

2010-11-18 | E-GEOD-25125 | biostudies-arrayexpress

Transcription profiling of human monocytes from patients with dominant negative mutations in PPARg and rosiglitazone treated cells to investigate PPARg regulated gene expression in human dendritic cells

Project description:In order to gain insights into how PPARg regulates different facets of dendritic cell (DC) differentiation, we sought to identify PPARg regulated genes and gene networks in monocyte-derived dendritic cells using global gene expression profiling. We employed an exogenous ligand activation approach using a selective PPARg ligand (rosiglitazone abbreviated as RSG). In addition, we have defined culture conditions in which human serum (HS) induces PPARg activation via a yet uncharacterized endogenous mechanism. We also compared the gene expression profile of developing dendritic cells obtained from patients harboring dominant negative mutations of the PPARg receptor (C114R and C131Y). Experiment Overall Design: Monocytes were cultured for 6, 24 hours or 5 days with 500 U/ml IL-4 and 800 U/ml GM-CSF; cytokine treatment was repeated at day 3. Cells were obtained from 12 healthy individuals (6 biological replicates; the 6 and 24 hours samples were obtained from a single individual but the 5 days samples from a different one). Ligands were added at the beginning of differentiation. The 6 and 24 hours cells were treated with vehicle (DC) or 1 uM rosiglitazone (DC RSG), in the case of 5 day cultured cells 2.5 uM RSG was used. Cells were cultured in RPMI plus 10% FBS, in the case of DC4-DC6 cells were also cultured in human AB serum (DC HS). Finally we also obtained cells from patients harboring point mutations of the PPARg receptor (C114R and C131Y)

2008-06-16 | E-GEOD-8658 | biostudies-arrayexpress

PPARg and IL-4-induced gene expression data from PPARg +/- LysCre and PPARg fl/- LysCre mouse bone marrow-derived alternatively activated macrophages and immature dendritic cells (iDCs)

Project description:Conditional macrophage-specific PPARg knockout mice were generated on C57Bl/6 background by breeding PPARg fl/- (one allele is floxed, the other is null) and lysozyme Cre transgenic mice. PPARg and IL-4 signaling was analyzed on bone marrow-derived macrophages. Bone marrow of 4 mice per group was isolated and differentiated to alternatively activated macrophages with 20 ng/ml M-CSF and 20 ng/ml IL-4 or to iDCs with 20 ng/ml GM-CSF+20 ng/ml IL-4. 1 uM Rosiglitazone (RSG) was used to activate PPARg. From each mouse 4 samples were generated: 1. M-CSF+IL-4, 2. M-CSF+IL-4+RSG, 3. GM-CSF+IL-4 and 4. GM-CSF+IL-4+RSG. All compounds were added throughout the whole differentiation process, and fresh media was added every other day. Control cells were treated with vehicle (DMSO:ethanol). After 9 days, RNA was isolated and gene expression profiles were analyzed using ABI Mouse Genome Survey Arrays.

2010-11-18 | GSE25125 | GEO

Identification of gene expression changes induced by ligands for RXR and its partners in differentiating human monocyte-derived dendritic cells

Project description:Differentiating human dendritic cells were stimulated for 12 hours with RXR agonists (LG268, 9CRA, R- and S-9CDHRA) or agonists for RXR partners including GW3965 (LXRα/β panagonist), RSG (PPARγ agonist), and GW1516 (PPARδ agonist) and AM580 (RARa agonist). The gene expression changes were detected globally by Affymetrix Human Genome U133 Plus 2.0 Arrays.

2015-06-04 | GSE48573 | GEO

PPARg and IL-4-induced gene expression data from wild-type and STAT6 knockout mouse bone marrow-derived macrophages

Project description:C57Bl/6 wild-type and STAT6 KO mice were used to study PPARg and IL-4 signaling. Bone marrow of 3 mice per group was isolated and differentiated to macrophages with M-CSF (20 ng/ml). 20 ng/ml IL-4 was used to induce alternative macrophage activation and 1 uM Rosiglitazone (RSG) was used to activate PPARg. From each mouse 4 samples were generated: 1. M-CSF, 2. M-CSF+RSG, 3. IL-4 and 4. IL-4+RSG. All compounds were added throughout the whole differentiation process, and frech media was added every other day. Control cells were treated with vehicle (DMSO:ethanol). After 10 days, RNA was isolated and gene expression profiles were analyzed using Mouse Genome 430 2.0 microarrays from Affymetrix.

2010-11-18 | GSE25088 | GEO

PPARg and IL-4-induced gene expression data from wild-type and STAT6 knockout mouse bone marrow-derived macrophages

2010-11-18 | E-GEOD-25088 | biostudies-arrayexpress