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Genome-wide binding of STAT3 in peritoneal macrophages

ABSTRACT: To try to identify the mechanism of STAT3âs indirect action we have used a genomic approach to map the binding sites of STAT3 within the genome and also used RNA-seq technology to map the changes in RNA expression and transcript isoforms in response to IL-10. Examination of STAT3 binding by ChIP-seq in Unstimulated and IL-10 treated peritoneal exudate macrophages purified from mice. We sequenced anti-STAT3 ChIP-seq as well as corresponding control (Input) libraries

ORGANISM(S): Mus musculus

SUBMITTER: Andrew Hutchins

PROVIDER: E-GEOD-31529 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide analysis of STAT3 binding in vivo predicts effectors of the anti-inflammatory response in macrophages.

Hutchins Andrew Paul AP Poulain Stéphane S Miranda-Saavedra Diego D

Blood 20120209 13

Inflammation is a powerful response of the immune system against invading pathogens, and must be cancelled when unneeded or otherwise death inevitably follows. In macrophages, the anti-inflammatory response (AIR) is driven by STAT3 upon IL-10 signaling. The role of STAT3 is to stimulate the expression of specific genes that in-turn suppress the transcription of proinflammatory genes. Here we describe a systematic approach to identify the elusive STAT3-controlled effectors of the AIR. In vivo STA ...[more]

PMID: 22323479

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Genome-wide analysis of STAT3-binding and gene expression changes in peritoneal macrophages upon interleukin-10 stimulation

Project description:This SuperSeries is composed of the following subset Series: GSE31529: Genome-wide binding of STAT3 in peritoneal macrophages GSE31530: Transcriptome changes in IL-10 treated peritoneal macrophages Refer to individual Series

2012-02-13 | E-GEOD-31531 | biostudies-arrayexpress

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MicroRNA expression in thioglycollate and alternatively activated

Project description:Macrophage activation must be tightly controlled to prevent overzealous responses that cause self-damage. MicroRNAs have been shown to promote classical macrophage activation by blocking concomitant anti-inflammatory signals and transcription factors, but can also place restraints on activation by preventing excessive TLR-signalling. In contrast, the microRNA profile associated with alternatively activated macrophages and their role in regulating wound-healing or anti-helminthic responses has not yet been described. Utilizing an in vivo model of alternative activation, in which adult Brugia malayi nematodes are surgically implanted in the peritoneal cavity of mice, we examined the profile of microRNA expression in these alternatively activated macrophages and compared this to alternatively activated IL-4 receptor knockout macrophages and thioglycollate elicited macrophages. Peritoneal macrophages from BALB/c wild type or IL-4 receptor knockout mice were elicited with thioglycollate or using nemtodes (peritoneal implant of Brugia malayi). The latter leads to a population of alternatively activated macrophages. Microarray analysis was used to examine the microRNA profile of WT alternatively activated macrophages (n = 4), IL-4 receptor knockout alternatively activated macrophages (n = 4), WT thioglycollate elicited macrophages (n = 3) and IL-4 receptor knockout thioglycollate elicited macrophages (n = 3).

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Transcriptional profiling in macrophages in stimulated and unstimulated conditions.

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