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Characterization of transcriptional and epigenetic changes during mouse alternative macrophage polarization [ChIP-Seq I]

ABSTRACT: The molecular basis of signal-dependent transcriptional activation has been extensively studied in macrophage polarization, however our understanding remains limited regarding the molecular determinants of repression. Here we showed that IL-4-activated STAT6 transcription factor is required for the direct transcriptional repression of a large number of genes during mouse alternative macrophage polarization. Repression results in decreased lineage-determining transcription factor, p300 coactivator and RNA polymerase II binding followed by reduced enhancer RNA expression, H3K27 acetylation and chromatin accessibility. In addition, STAT6-repressed enhancers showed extensive overlap with the NF-κB p65 transcription factor cistrome and exhibited decreased responsiveness to lipopolysaccharide after IL-4 stimulus on a subset of genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE106701 | GEO | 2017/11/10

REPOSITORIES: GEO

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Characterization of transcriptional and epigenetic changes during mouse alternative macrophage polarization [ATAC-Seq]

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Project description:Macrophages change their phenotype in response to complex (reinforcing or opposing) environmental cues. The molecular components providing the epigenomic basis of progressive or reinforcing polarization are largely unknown. Here we show that the normally ligand-activated nuclear receptor, Peroxisome Proliferator-Activated Receptor gamma (PPARγ), is a predominantly ligand-insensitive, epigenomic driver of a robust phenotypic change in macrophages uniquely upon repeated/reinforcing IL-4 stimulation. Ligand-insensitive PPARγ recruits P300, RAD21 and establishes a permissive chromatin environment, conferring transcriptional memory by facilitating the binding of STAT6 and RNAPII leading to more robust eRNA production upon IL-4 restimulation. PPARγ-mediated transcriptional memory allows the progressive, functional transition of macrophages upon repeated cytokine exposure by controlling the expression of an extracellular matrix remodeling related gene network, also expressed in macrophages from a mouse model of muscle regeneration and show progressive upregulation during the course of regeneration after muscle injury, coinciding with the appearance of IL-4 and PPARγ. Collectively, in contrast to the current prevailing view, alternative polarization gives rise to a predominantly ligand-insensitive PPARγ:RXR cistrome, regulating progressive/reinforcing macrophage polarization.

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