Abstract
Macrophages exert a wide variety of functions, which necessitate a high level of plasticity on the chromatin level. In the work presented here, we analyzed the role of the polycomb group protein Bmi1 during the acute response of bone marrow derived macrophages (BMDM) to lipopolysaccharide (LPS). Unexpectedly, we observed that Bmi1 was rapidly induced at the protein level and transiently phosphorylated upon LPS treatment. The induction of Bmi1 was dependent on MAP-kinase signaling. LPS treatment of BMDM in the absence of Bmi1 resulted in a pronounced increase in expression of the anti-inflammatory cytokine interleukin-10 (IL-10). Our results identify Bmi1 as a repressor of IL-10 expression during macrophage activation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Line
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Interleukin-10 / biosynthesis*
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Interleukin-10 / metabolism
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Lipopolysaccharides / immunology
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MAP Kinase Signaling System
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Macrophage Activation* / immunology
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Macrophages / immunology*
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Macrophages / metabolism
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Mice
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Mice, Transgenic
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Mitogen-Activated Protein Kinases / metabolism
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Nuclear Proteins / metabolism*
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Polycomb Repressive Complex 1
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Proto-Oncogene Proteins / metabolism*
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RNA Interference
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RNA, Small Interfering
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Repressor Proteins / metabolism*
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Toll-Like Receptor 4 / metabolism
Substances
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Bmi1 protein, mouse
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Lipopolysaccharides
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Nuclear Proteins
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Proto-Oncogene Proteins
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RNA, Small Interfering
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Repressor Proteins
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Tlr4 protein, mouse
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Toll-Like Receptor 4
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Interleukin-10
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Polycomb Repressive Complex 1
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Mitogen-Activated Protein Kinases