MKL1 defines the H3K4Me3 landscape for NF-κB dependent inflammatory response

Macrophage-dependent inflammatory response is considered a pivotal biological process that contributes to a host of diseases when aberrantly activated. The underlying epigenetic mechanism is not completely understood. We report here that MKL1 was both sufficient and necessary for p65-dependent pro-i...

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Published inScientific reports Vol. 7; no. 1; p. 191
Main Authors Yu, Liming, Fang, Fei, Dai, Xin, Xu, Huihui, Qi, Xiaohong, Fang, Mingming, Xu, Yong
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 15.03.2017
Nature Portfolio
Subjects
38/15
38/61
38/77
38/89
631/250/256/1980
631/337/176
631/337/572/2102
Animals
Cells, Cultured
Chromatin Immunoprecipitation
Disease Models, Animal
Epigenesis, Genetic
Gene Expression Profiling
Gene Expression Regulation
Histone-Lysine N-Methyltransferase - metabolism
Histones - metabolism
Humanities and Social Sciences
Humans
Lipopolysaccharides - administration & dosage
Macrophages, Peritoneal - cytology
Macrophages, Peritoneal - immunology
Macrophages, Peritoneal - metabolism
Methylation
Mice
multidisciplinary
Science
Science (multidisciplinary)
Shock, Septic - chemically induced
Shock, Septic - genetics
Shock, Septic - metabolism
THP-1 Cells
Trans-Activators - genetics
Trans-Activators - metabolism
Transcription Factor RelA - metabolism
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Abstract Macrophage-dependent inflammatory response is considered a pivotal biological process that contributes to a host of diseases when aberrantly activated. The underlying epigenetic mechanism is not completely understood. We report here that MKL1 was both sufficient and necessary for p65-dependent pro-inflammatory transcriptional program in immortalized macrophages, in primary human and mouse macrophages, and in an animal model of systemic inflammation (endotoxic shock). Extensive chromatin immunoprecipitation (ChIP) profiling and ChIP-seq analyses revealed that MKL1 deficiency erased key histone modifications synonymous with transactivation on p65 target promoters. Specifically, MKL1 defined histone H3K4 trimethylation landscape for NF-κB dependent transcription. MKL1 recruited an H3K4 trimethyltransferase SET1 to the promoter regions of p65 target genes. There, our work has identified a novel modifier of p65-dependent pro-inflammatory transcription, which may serve as potential therapeutic targets in treating inflammation related diseases.
AbstractList Macrophage-dependent inflammatory response is considered a pivotal biological process that contributes to a host of diseases when aberrantly activated. The underlying epigenetic mechanism is not completely understood. We report here that MKL1 was both sufficient and necessary for p65-dependent pro-inflammatory transcriptional program in immortalized macrophages, in primary human and mouse macrophages, and in an animal model of systemic inflammation (endotoxic shock). Extensive chromatin immunoprecipitation (ChIP) profiling and ChIP-seq analyses revealed that MKL1 deficiency erased key histone modifications synonymous with transactivation on p65 target promoters. Specifically, MKL1 defined histone H3K4 trimethylation landscape for NF-κB dependent transcription. MKL1 recruited an H3K4 trimethyltransferase SET1 to the promoter regions of p65 target genes. There, our work has identified a novel modifier of p65-dependent pro-inflammatory transcription, which may serve as potential therapeutic targets in treating inflammation related diseases.
Abstract Macrophage-dependent inflammatory response is considered a pivotal biological process that contributes to a host of diseases when aberrantly activated. The underlying epigenetic mechanism is not completely understood. We report here that MKL1 was both sufficient and necessary for p65-dependent pro-inflammatory transcriptional program in immortalized macrophages, in primary human and mouse macrophages, and in an animal model of systemic inflammation (endotoxic shock). Extensive chromatin immunoprecipitation (ChIP) profiling and ChIP-seq analyses revealed that MKL1 deficiency erased key histone modifications synonymous with transactivation on p65 target promoters. Specifically, MKL1 defined histone H3K4 trimethylation landscape for NF-κB dependent transcription. MKL1 recruited an H3K4 trimethyltransferase SET1 to the promoter regions of p65 target genes. There, our work has identified a novel modifier of p65-dependent pro-inflammatory transcription, which may serve as potential therapeutic targets in treating inflammation related diseases.
Abstract Macrophage-dependent inflammatory response is considered a pivotal biological process that contributes to a host of diseases when aberrantly activated. The underlying epigenetic mechanism is not completely understood. We report here that MKL1 was both sufficient and necessary for p65-dependent pro-inflammatory transcriptional program in immortalized macrophages, in primary human and mouse macrophages, and in an animal model of systemic inflammation (endotoxic shock). Extensive chromatin immunoprecipitation (ChIP) profiling and ChIP-seq analyses revealed that MKL1 deficiency erased key histone modifications synonymous with transactivation on p65 target promoters. Specifically, MKL1 defined histone H3K4 trimethylation landscape for NF-κB dependent transcription. MKL1 recruited an H3K4 trimethyltransferase SET1 to the promoter regions of p65 target genes. There, our work has identified a novel modifier of p65-dependent pro-inflammatory transcription, which may serve as potential therapeutic targets in treating inflammation related diseases.
ArticleNumber 191
Author Xu, Yong
Qi, Xiaohong
Fang, Fei
Yu, Liming
Dai, Xin
Xu, Huihui
Fang, Mingming
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Snippet Macrophage-dependent inflammatory response is considered a pivotal biological process that contributes to a host of diseases when aberrantly activated. The...
Abstract Macrophage-dependent inflammatory response is considered a pivotal biological process that contributes to a host of diseases when aberrantly...
Abstract Macrophage-dependent inflammatory response is considered a pivotal biological process that contributes to a host of diseases when aberrantly...
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SubjectTerms 38/15
38/61
38/77
38/89
631/250/256/1980
631/337/176
631/337/572/2102
Animals
Cells, Cultured
Chromatin Immunoprecipitation
Disease Models, Animal
Epigenesis, Genetic
Gene Expression Profiling
Gene Expression Regulation
Histone-Lysine N-Methyltransferase - metabolism
Histones - metabolism
Humanities and Social Sciences
Humans
Lipopolysaccharides - administration & dosage
Macrophages, Peritoneal - cytology
Macrophages, Peritoneal - immunology
Macrophages, Peritoneal - metabolism
Methylation
Mice
multidisciplinary
Science
Science (multidisciplinary)
Shock, Septic - chemically induced
Shock, Septic - genetics
Shock, Septic - metabolism
THP-1 Cells
Trans-Activators - genetics
Trans-Activators - metabolism
Transcription Factor RelA - metabolism
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Title MKL1 defines the H3K4Me3 landscape for NF-κB dependent inflammatory response
URI https://link.springer.com/article/10.1038/s41598-017-00301-w
https://www.ncbi.nlm.nih.gov/pubmed/28298643
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https://pubmed.ncbi.nlm.nih.gov/PMC5428227
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