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Niche-Specific Re-Programming of Epigenetic Landscapes Drives Myeloid Cell Diversity in NASH

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

ORGANISM(S): Mus musculus

PROVIDER: GSE128338 | GEO | 2020/05/05

REPOSITORIES: GEO

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Niche-Specific Re-Programming of Epigenetic Landscapes Drives Myeloid Cell Diversity in NASH [ChIP-seq]

Project description:Tissue resident macrophages and recruited monocyte-derived macrophages contribute to host defense but also play pathological roles in a diverse range of human diseases. Multiple macrophage phenotypes are often represented in a diseased tissue, but we lack a deep understanding of the mechanisms that control diversification. Here we use a combination of genetic, genomic, and imaging approaches to investigate the origins and epigenetic trajectories of hepatic myeloid cells during a diet-induced model of nonalcoholic steatohepatitis (NASH). We provide evidence that distinct microenvironments within the NASH liver induce strikingly divergent transcriptomes of resident and infiltrating cells. Myeloid cell diversification results from both remodeling open chromatin landscapes of recruited monocytes and altering activities of preexisting enhancers of resident Kupffer cells. These findings provide evidence that niche-specific combinations of disease-associated environmental signals instruct resident and recruited macrophages to acquire distinct programs of gene expression and corresponding phenotypes.

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Niche-Specific Re-Programming of Epigenetic Landscapes Drives Myeloid Cell Diversity in NASH [ATAC-seq]

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Niche-Specific Re-Programming of Epigenetic Landscapes Drives Myeloid Cell Diversity in NASH [scRNA-seq]

Project description:Tissue resident macrophages and recruited monocyte-derived macrophages contribute to host defense but also play pathological roles in a diverse range of human diseases. Multiple macrophage phenotypes are often represented in a diseased tissue, but we lack a deep understanding of the mechanisms that control diversification. Here we use a combination of genetic, genomic, and imaging approaches to investigate the origins and epigenetic trajectories of hepatic myeloid cells during a diet-induced model of nonalcoholic steatohepatitis (NASH). We provide evidence that distinct micro-environments within the NASH liver induce strikingly divergent transcriptomes of resident and infiltrating cells. Myeloid cell diversification results from both remodeling open chromatin landscapes of recruited monocytes and altering activities of pre-existing enhancers of resident Kupffer cells. These findings provide evidence that niche-specific combinations of diseaseassociated environmental signals instruct resident and recruited macrophages to acquire distinct programs of gene expression and corresponding phenotypes.

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Niche-Specific Re-Programming of Epigenetic Landscapes Drives Myeloid Cell Diversity in NASH [RNA-seq]

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Niche-Specific Re-Programming of Epigenetic Landscapes Drives Myeloid Cell Diversity in NASH

Project description:Niche-Specific Re-Programming of Epigenetic Landscapes Drives Myeloid Cell Diversity in NASH

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Niche-Specific Reprogramming of Epigenetic Landscapes Drives Myeloid Cell Diversity in Nonalcoholic Steatohepatitis.

Project description:Tissue-resident and recruited macrophages contribute to both host defense and pathology. Multiple macrophage phenotypes are represented in diseased tissues, but we lack deep understanding of mechanisms controlling diversification. Here, we investigate origins and epigenetic trajectories of hepatic macrophages during diet-induced non-alcoholic steatohepatitis (NASH). The NASH diet induced significant changes in Kupffer cell enhancers and gene expression, resulting in partial loss of Kupffer cell identity, induction of Trem2 and Cd9 expression, and cell death. Kupffer cell loss was compensated by gain of adjacent monocyte-derived macrophages that exhibited convergent epigenomes, transcriptomes, and functions. NASH-induced changes in Kupffer cell enhancers were driven by AP-1 and EGR that reprogrammed LXR functions required for Kupffer cell identity and survival to instead drive a scar-associated macrophage phenotype. These findings reveal mechanisms by which disease-associated environmental signals instruct resident and recruited macrophages to acquire distinct gene expression programs and corresponding functions.

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Niche-Specific Re-Programming of Epigenetic Landscapes Drives Myeloid Cell Diversity in NASH [ATAC-seq]

Project description:Niche-Specific Re-Programming of Epigenetic Landscapes Drives Myeloid Cell Diversity in NASH [ATAC-seq]

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Niche-Specific Re-Programming of Epigenetic Landscapes Drives Myeloid Cell Diversity in NASH [scRNA-seq]

Project description:Niche-Specific Re-Programming of Epigenetic Landscapes Drives Myeloid Cell Diversity in NASH [scRNA-seq]

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Niche-Specific Re-Programming of Epigenetic Landscapes Drives Myeloid Cell Diversity in NASH [RNA-seq]

Project description:Niche-Specific Re-Programming of Epigenetic Landscapes Drives Myeloid Cell Diversity in NASH [RNA-seq]

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Niche-Specific Re-Programming of Epigenetic Landscapes Drives Myeloid Cell Diversity in NASH [ChIP-seq]

Project description:Niche-Specific Re-Programming of Epigenetic Landscapes Drives Myeloid Cell Diversity in NASH [ChIP-seq]