Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-5679
PROVIDER: PRJNA96965 | ENA |
REPOSITORIES: ENA
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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. Keywords: ligand response
2006-09-19 | GSE5679 | GEO
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).
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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). Keywords: ligand response
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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)
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