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Histone methyltransferase DOT1L regulates macrophage lipid biosynthesis and inflammatory responses and affects atherosclerotic plaque stability [RNA-seq III]

ABSTRACT: Histone methyltransferase DOT1L regulates macrophage lipid biosynthesis and inflammatory responses and affects atherosclerotic plaque stability [RNA-seq III]

PROVIDER: PRJNA876265 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21642046.fastq.gz	Fastqsanger.gz
	SRR21642047.fastq.gz	Fastqsanger.gz
	SRR21642048.fastq.gz	Fastqsanger.gz
	SRR21642049.fastq.gz	Fastqsanger.gz
	SRR21642050.fastq.gz	Fastqsanger.gz

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Histone methyltransferase DOT1L regulates macrophage lipid biosynthesis and inflammatory responses and affects atherosclerotic plaque stability [RNA-seq III]

Project description:Macrophages are critical immune cells in inflammatory diseases and their differentiation and function are tightly regulated by epigenetic alterations. H3K79 methylation is an epigenetic modification associated with active gene expression and DOT1L is the only histone methyltransferase for H3K79. Here we determine the role of DOT1L in macrophages by applying a selective DOT1L inhibitor in mouse and human macrophages and using myeloid-specific Dot1l deficient mice. We found that DOT1L directly regulates macrophage function by controlling lipid biosynthesis gene programs including central lipid regulators like sterol regulatory element-binding proteins SREBP1 and SREBP2. DOT1L inhibition also leads to macrophage hyperactivation which is associated with disrupted SREBP pathways. In vivo, myeloid Dot1l deficiency reduces atherosclerotic plaque stability and increases the activation of inflammatory plaque macrophages. Our data show that DOT1L is a crucial regulator of macrophage inflammatory responses and lipid regulatory pathways and suggests a high relevance of H3K79 methylation in inflammatory disease.

2022-10-04 | GSE212563 | GEO

Histone methyltransferase DOT1L regulates macrophage lipid biosynthesis and inflammatory responses and affects atherosclerotic plaque stability [ChIP-seq]

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Histone methyltransferase DOT1L regulates macrophage lipid biosynthesis and inflammatory responses and affects atherosclerotic plaque stability [ChIP-seq II]

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Histone methyltransferase DOT1L regulates macrophage lipid biosynthesis and inflammatory responses and affects atherosclerotic plaque stability [RNA-seq II]

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Histone methyltransferase DOT1L regulates macrophage lipid biosynthesis and inflammatory responses and affects atherosclerotic plaque stability

Project description:Histone methyltransferase DOT1L regulates macrophage lipid biosynthesis and inflammatory responses and affects atherosclerotic plaque stability

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Histone methyltransferase DOT1L regulates macrophage lipid biosynthesis and inflammatory responses and affects atherosclerotic plaque stability [ChIP-seq]

Project description:Histone methyltransferase DOT1L regulates macrophage lipid biosynthesis and inflammatory responses and affects atherosclerotic plaque stability [ChIP-seq]

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Histone methyltransferase DOT1L regulates macrophage lipid biosynthesis and inflammatory responses and affects atherosclerotic plaque stability [RNA-seq II]

Project description:Histone methyltransferase DOT1L regulates macrophage lipid biosynthesis and inflammatory responses and affects atherosclerotic plaque stability [RNA-seq II]

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Histone methyltransferase DOT1L regulates macrophage lipid biosynthesis and inflammatory responses and affects atherosclerotic plaque stability [ChIP-seq II]

Project description:Histone methyltransferase DOT1L regulates macrophage lipid biosynthesis and inflammatory responses and affects atherosclerotic plaque stability [ChIP-seq II]

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Gene expression profiling of human atherosclerotic plaque

Project description:This SuperSeries is composed of the following subset Series: GSE23303: Gene expression profiling of human atherosclerotic plaque: Laser capture microscopy of smooth muscle cells and macrophages GSE23304: Gene expression profiling of human atherosclerotic plaque: 101 peripheral plaques GSE24495: Gene expression profiling of human atherosclerotic plaque: Carotid plaque GSE24702: Gene expression profiling of human atherosclerotic plaque: 290 peripheral plaques Refer to individual Series

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Project description:The rupture of unstable atherosclerotic plaques, leading to debilitating or fatal thrombotic events, is a major health burden worldwide. Limited understanding as to the molecular drivers of plaque instability and rupture hinders efforts in diagnosis and treatment prior to thrombotic events. Utilising an advanced pre-clinical mouse model (Tandem stenosis (TS) model), which presents human-like unstable atherosclerotic disease, we apply high-end omic methods to characterize the molecular signatures associated with plaque instability in atherosclerotic arteries. Through quantitative proteomic profiling, we depict unique proteome signatures of unstable plaques compared to stable plaques and healthy arteries. Coupled with single-cell RNA-sequencing of leukocytes, we describe the heterodimer complex S100a8/S100a9 as unique to unstable plaque, with neutrophils implicated as the transcriptional drivers of S100a8/a9 expression. We confirm S100a9 expression in human carotid atherosclerotic plaques and we further utilise the TS pre-clinical model to pharmacologically inhibit S100a8/S100a9, resulting in plaque stabilisation. Thus, we establish the TS model as a sophisticated translational tool for the profiling of unstable atherosclerotic plaques and demonstrate that unstable and stable atherosclerosis are highly different disease entities.

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