Characterization of transcriptional and epigenetic changes during mouse alternative macrophage polarization
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PROVIDER: PRJNA417710 | ENA |
REPOSITORIES: ENA
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Project description: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.
2017-11-10 | GSE106703 | GEO
Project description: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.
2017-11-10 | GSE106702 | GEO
Project description: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.
2017-11-10 | GSE106700 | GEO
Project description: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.
2017-11-10 | GSE106705 | GEO
Project description: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.
2017-11-10 | GSE106704 | GEO
Project description: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.
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Project description:In response to microenvironmental signals macrophages undergo different activation, indicated as classic/M1 and alternative/M2 polarization. C-Myc transcription factor could be an essential player in M2 polarization. Functional relevance of c-Myc in M2 macrophage biology is investigated by evaluating the effect of 100-58F4, on the transcriptional profile induced on human macrophages by IL-4. Human monocytes were obtained from normal donor buffy coats by two-step gradient centrifugation using Ficoll (Biochrom) and Percoll (Amersham). Non-adherent cells were discarded, and the purified monocytes were incubated for 7 days in RPMI 1640 (Biochom) supplemented with 10% FCS (HyClone) and 100 ng/mL M-CSF to obtain resting macrophages. Macrophage polarization was obtained by removing the culture medium and culturing cells in RPMI 1640 supplemented with 10% FCS and 100 ng/mL LPS plus 20 ng/mL IFN-gamma (M1 polarization) or 20 ng/mL IL-4 (M2 polarization) for 24 h. When needed, chemical inhibitors were added with IL-4.
2011-09-15 | E-GEOD-32164 | biostudies-arrayexpress
Project description:In response to microenvironmental signals macrophages undergo different activation, indicated as classic/M1 and alternative/M2 polarization. C-Myc transcription factor could be an essential player in M2 polarization. Functional relevance of c-Myc in M2 macrophage biology is investigated by evaluating the effect of 100-58F4, on the transcriptional profile induced on human macrophages by IL-4.
2011-09-16 | GSE32164 | GEO
Project description:Hyperuricemia is an essential risk factor in chronic kidney disease (CKD), while urate-lowering therapy to prevent or delay CKD is controversial. Alternatively activated macrophages in response to local microenvironment play diverse roles in kidney diseases. Here, we aim to investigate whether and how macrophage integrin αM (ITGAM) contributes to hyperuricemia-related CKD. In vivo, we explored dynamic characteristics of renal tissue in C57BL/6J mice with hyperuricemia-related CKD. By incorporating transcriptomics and phosphoproteomics data, we analyzed gene expression profile, hub genes and potential pathways. In vitro, we validated bioinformatic findings under different conditions with interventions corresponding to core nodes. We found that hyperuricemia-related CKD was characterized by elevated serum uric acid levels, impaired renal function, activation of macrophage alternative (M2) polarization, and kidney fibrosis. Integrated bioinformatic analyses revealed Itgam as the potential core gene and was associated with focal adhesion signaling. Notably, we confirmed the upregulated expression of macrophage ITGAM, activated pathway, and macrophage M2 polarization in injured kidneys. In vitro, through silencing Itgam, inhibiting p-FAK or p-AKT1 phosphorylation, and concurrent inhibiting of p-FAK while activating p-AKT1 all contributed to the modulation of macrophage M2 polarization. Our results indicated targeting macrophage ITGAM might be a promising therapeutic approach for preventing CKD.
2024-06-26 | GSE262687 | GEO
Project description:Small Noncoding RNAome Changes during macrophage polarization
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