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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Licensing of PPARg-regulated gene expression by IL-4-induced alternative macrophage activation

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE16385: Expression data from human macrophages GSE16386: Expression data from human alternatively activated macrophages GSE25088: PPARg and IL-4-induced gene expression data from wild-type and STAT6 knockout mouse bone marrow-derived macrophages GSE25123: PPARg and IL-4-induced gene expression data from PPARg +/- LysCre and PPARg fl/- LysCre mouse bone marrow-derived macrophages GSE25125: 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) Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Attila Szanto

PROVIDER: E-GEOD-16387 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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STAT6 transcription factor is a facilitator of the nuclear receptor PPARγ-regulated gene expression in macrophages and dendritic cells.

Szanto Attila A Balint Balint L BL Nagy Zsuzsanna S ZS Barta Endre E Dezso Balazs B Pap Attila A Szeles Lajos L Poliska Szilard S Oros Melinda M Evans Ronald M RM Barak Yaacov Y Schwabe John J Nagy Laszlo L

Immunity 20101101 5

Peroxisome proliferator-activated receptor γ (PPARγ) is a lipid-activated transcription factor regulating lipid metabolism and inflammatory response in macrophages and dendritic cells (DCs). These immune cells exposed to distinct inflammatory milieu show cell type specification as a result of altered gene expression. We demonstrate here a mechanism how inflammatory molecules modulate PPARγ signaling in distinct subsets of cells. Proinflammatory molecules inhibited whereas interleukin-4 (IL-4) st ...[more]

PMID: 21093321

Similar Datasets

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 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

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. 3 C57Bl/6 wild-type and 3 STAT6 KO 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-25088 | biostudies-arrayexpress

Expression data from human macrophages

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2010-11-18 | E-GEOD-16385 | biostudies-arrayexpress

Expression data from human alternatively activated macrophages

Project description:Human CD14 positive monocytes were purified from healthy volunteers’ blood and cultured in vitro for 6 hours. While culturing, macrophages were activated alternatively with interleukin-4 (IL-4 100 ng/ml). Simultaneously, macrophages were also treated with vehicle (DMSO:ethanol) or 1uM synthetic PPARg agonist, Rosiglitazone. We used Affymetrix microarrays (U133Plus 2.0) to analyze activation and PPARg-induced gene expression changes. Monocytes from 2 donors were used and treated as indicated in Summary. Technical replicates were generated from each sample.

2010-11-18 | E-GEOD-16386 | 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

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

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

Reprogramming of primary human Philadelphia chromosome-positive B cell acute lymphoblastic leukemia cells into nonleukemic macrophages

Project description:BCR–ABL1+ precursor B-cell acute lymphoblastic leukemia (BCR– ABL1+ B-ALL) is an aggressive hematopoietic neoplasm characterized by a block in differentiation due in part to the somatic loss of transcription factors required for B-cell development. We hypothesized that overcoming this differentiation block by forcing cells to reprogram to the myeloid lineage would reduce the leukemogenicity of these cells. We found that primary human BCR–ABL1+ B-ALL cells could be induced to reprogram into macrophage-like cells by exposure to myeloid differentiation-promoting cytokines in vitro or by transient expression of the myeloid transcription factor C/EBPα or PU.1. The resultant cells were clonally related to the primary leukemic blasts but resembled normal macrophages in appearance, immunophenotype, gene expression, and function. Most importantly, these macrophage-like cells were unable to establish disease in xenograft hosts, indicating that lineage reprogramming eliminates the leukemogenicity of BCR–ABL1+ B-ALL cells, and suggesting a previously unidentified therapeutic strategy for this disease. Finally, we determined that myeloid reprogramming may occur to some degree in human patients by identifying primary CD14+ monocytes/ macrophages in BCR–ABL1+ B-ALL patient samples that possess the BCR–ABL1+ translocation and clonally recombined VDJ regions. We obtained the expression profiles of 5 human B-ALL samples using Afymmetrix U133A2 microarrays. Blasts were either analyzed without culture, or cultured in the presence of myeloid cytokines and sorted into CD14+ and CD19+ populations.

2015-04-01 | E-GEOD-66792 | biostudies-arrayexpress

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2011-12-01 | E-GEOD-25426 | biostudies-arrayexpress

Transcription profiling of human DC and macrophages stimulated with Mycobacterium Tuberculosis

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