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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE193119 | GEO | 2022/10/04

REPOSITORIES: GEO

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

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 | GSE183043 | GEO

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

2022-10-04 | GSE212563 | GEO

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

2022-10-04 | GSE211874 | GEO

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

2022-10-04 | GSE193529 | GEO

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

| PRJNA794851 | ENA

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]

| PRJNA758930 | ENA

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

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

| PRJNA876265 | ENA

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]

| PRJNA796543 | ENA

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]

| PRJNA872479 | ENA

Ginsenoside Rb1 Enhances Atherosclerotic Plaque Stability by Improving Autophagy and Lipid Metabolism in Macrophage Foam Cells.

Project description:Atherosclerosis (AS) is a lipid-driven disease in which macrophage foam cells play a critical role by increasing vascular lipid accumulation and contributing to plaque instability. Ginsenoside Rb1 (Rb1), the most abundant active component of ginseng, has been found potently to promote lipid metabolism and attenuate lipid accumulation. However, the underlying mechanisms remain unclear. In this study, the effects of Rb1 on lipid accumulation and plaque stability were investigated both in vitro and in vivo by using primary peritoneal macrophages isolated from C57BL/6 mice and an AS model in ApoE-/- mice. The results showed that Rb1 reduced lipid accumulation both in macrophage foam cells and atherosclerotic plaques. Rb1 treatment promoted plaque stability by modifying plaque composition via the activation of autophagy both in vitro and in vivo. Transmission electron microscopy further showed an increased accumulation of autophagolysosomes in Rb1-treated macrophage foam cells. However, the modulation of lipid accumulation by Rb1 was attenuated by autophagy blockage using autophagy-related gene 5 (Atg5) small interfering RNA (siRNA) in vitro. In addition, Rb1 notably increased AMPK phosphorylation both in vitro and in vivo, and the AMPK inhibitor compound C abolished the Rb1-induced autophagy in macrophage foam cells. In conclusion, ginsenoside Rb1 reduced lipid accumulation in macrophage foam cells and enhanced atherosclerotic plaque stability by the induction of macrophage autophagy. Our study provides new evidence for the possible use of Rb1 in the prevention and treatment of AS.

| S-EPMC5660703 | biostudies-literature

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