Ontology highlight
ABSTRACT:
PROVIDER: PRJNA131203 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR063314.fastq.gz | Fastqsanger.gz | |||
| SRR063315.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 2 of 2 |
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Project description:Polarization of macrophages to M1 or M2 cells is important for mounting responses against bacterial and helminth infection respectively. Jumonji domain containing 3 (JMJD3), a histone 3 K27 demethylase, has been implicated in the activation of macrophages. Here we show that JMJD3 is essential for M2 macrophage polarization to helminth infection and chitin, though JMJD3 is dispensable for M1 responses. Furthermore, Jmjd3 is critical for proper bone marrow macrophage differentiation in a demethylase activity-dependent manner. Jmjd3 deficiency affected trimethylation of H3K27 in only a limited numbers of genes. Among them, we identified Irf4 as the target transcription factor critical for controlling M2 macrophage polarization. Collectively, these results show that JMJD3-mediated H3K27 demethylation is critical for regulating M2 macrophage development leading to anti-helminth host responses. This SuperSeries is composed of the SubSeries listed below.
2010-08-22 | GSE23306 | GEO
Project description:Jmjd3 is trimethyl H3K27 specific demethylase required for M2 macrophage polarization. Genomic fragments obtained from wild-type and Jmjd3-/- mouse macrophages were immunoprecipitated with anti H3K27me3 Ab, and deep sequencing was performed. wild-type and Jmjd3-/- macrophages
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Project description:MYC activates different metabolic programs in a cell-type and cell-status dependent manner. However, the role of MYC in inflammatory macrophages has not yet been determined. Metabolic and molecular analyses reveal that MYC, but not HIF1, is involved in enhancing early glycolytic flux during inflammatory macrophage polarization. Ablation of MYC decreases lactate production by regulating lactate dehydrogenase (LDH) activity and causes increased inflammatory cytokines by regulating interferon regulatory factor 4 (IRF4) in response to lipopolysaccharide (LPS). Moreover, myeloid-specific deletion of MYC and pharmacological inhibition of MYC/LDH axis enhance inflammation and the bacterial clearance in vivo. These results elucidate the potential role of the MYC/LDH/IRF4 axis in inflammatory macrophages by connecting early glycolysis and inflammatory responses and suggest that modulating early glycolytic flux mediated by the MYC/LDH axis can be utilized to open new avenues for the therapeutic modulation of macrophage polarization to fight against bacterial infection.
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Project description:Macrophage recruitment into tumors is correlated with poor outcomes in cancer, which correlate with STAT6-dependent M2 macrophage polarization and wound healing-type responses. Using penetrant, genetic models of neuroblastoma, we found macrophage recruitment was protective against tumor formation while disabling STAT6-mediated M2 polarization had no effect on tumorigenesis, progression or expression of key immunosuppressive pathways. Thus while macrophages are drivers of cancer in this model, non-classical M2 STAT6-independent pathways are plausible targets for cancer therapy.
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