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


ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Attila Szanto 

PROVIDER: E-GEOD-25088 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

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]

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