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The Histone Demethylase KDM6B Restrains Hypermetabolic LYVE1+ Perivascular Macrophages and Preserves Adipogenic Balance [CUT&Tag pvm]

ABSTRACT: We employed CUT&Tag sequencing to study H3K27me3 chromatin profiles in epididymal white adipose tissue perivascular macrophages isolated from wild-type and macrophage-specific KDM6B knockout mice fed a high-fat diet for 5 weeks. This study was designed to identify genotype-dependent changes in the repressive H3K27me3 mark associated with KDM6B deficiency during early diet-induced obesity.

ORGANISM(S): Mus musculus

PROVIDER: GSE338874 | GEO | 2026/09/01

REPOSITORIES: GEO

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The Histone Demethylase KDM6B Restrains Hypermetabolic LYVE1+ Perivascular Macrophages and Preserves Adipogenic Balance [ATAC-seq pvm]

Project description:We employed ATAC sequencing to study chromatin accessibility in adipose tissue perivascular macrophages isolated from wild-type and macrophage-specific KDM6B knockout mice fed a high-fat diet for 5 weeks. This study was designed to identify genotype-dependent changes in accessible chromatin regions associated with KDM6B deficiency during early diet-induced obesity. These data provide insights into regulatory elements controlling macrophage identity, inflammatory activation, lipid-associated macrophage states, and immune remodeling in obese adipose tissue.

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The Histone Demethylase KDM6B Restrains Hypermetabolic LYVE1+ Perivascular Macrophages and Preserves Adipogenic Balance

Project description:We employed bulk RNA sequencing to study adipose tissue macrophages isolated from epididymal white adipose tissue of wild-type and macrophage-specific KDM6B knockout mice fed a high-fat diet for 5 weeks. This study was designed to identify genotype-dependent transcriptional changes associated with KDM6B deficiency during early diet-induced obesity.

2026-09-01 | GSE339267 | GEO

The Histone Demethylase KDM6B Restrains Hypermetabolic LYVE1+ Perivascular Macrophages and Preserves Adipogenic Balance [scRNA-Seq]

Project description:We employed single-cell RNA sequencing to study adipose tissue macrophages isolated from epididymal white adipose tissue of wild-type and macrophage-specific KDM6B knockout mice fed a high-fat diet for 5 weeks. This study was designed to identify macrophage subpopulations and genotype-dependent transcriptional changes associated with KDM6B deficiency during early diet-induced obesity. These data provide insights into macrophage heterogeneity, inflammatory activation, lipid-associated macrophage states, and immune remodeling in obese adipose tissue.

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The Histone Demethylase KDM6B Restrains Hypermetabolic LYVE1+ Perivascular Macrophages and Preserves Adipogenic Balance [RNA-seq atm]

2026-09-01 | GSE338877 | GEO

The Histone Demethylase KDM6B Restrains Hypermetabolic LYVE1+ Perivascular Macrophages and Preserves Adipogenic Balance [RNA-seq wat]

Project description:We employed a bulk RNA sequencing approach to study transcriptional remodeling of white adipose tissue in wild-type and macrophage-specific KDM6B knockout mice fed a high-fat diet for 5 weeks. Subcutaneous white adipose tissue and epididymal white adipose tissue were collected and analyzed, with three biological replicates per group. This study was designed to identify depot-specific and genotype-dependent gene expression changes associated with diet-induced obesity. These data provide insights into macrophage-dependent regulation of adipose tissue inflammation, metabolic dysfunction, extracellular matrix remodeling, and tissue adaptation during chronic high-fat diet feeding.

2026-09-01 | GSE338875 | GEO

The Histone Demethylase KDM6B Restrains Hypermetabolic LYVE1+ Perivascular Macrophages and Preserves Adipogenic Balance [ATAC-Seq]

Project description:We employed ATAC sequencing to study chromatin accessibility in bone marrow-derived macrophages from wild-type and macrophage-specific KDM6B knockout mice following stimulation with LPS and IFNγ. This study was designed to identify genotype-dependent changes in accessible chromatin regions associated with inflammatory macrophage activation.

2026-09-01 | GSE338774 | GEO

The Histone Demethylase KDM6B Restrains Hypermetabolic LYVE1+ Perivascular Macrophages and Preserves Adipogenic

Project description:This SuperSeries is composed of the SubSeries listed below.

2026-09-01 | GSE338965 | GEO

Histone Demethylase KDM6B Promotes Postnatal Oligodendrocyte Development and Cortical Myelination

Project description:Myelination in the postnatal cortex requires epigenetic programs that activate oligodendrocyte gene networks. Here we show that the histone H3K27me3 demethylase KDM6B promotes this process in vivo. Conditional Kdm6b deletion (Kdm6b-cKO) in Emx1⁺ dorsal telencephalic progenitors caused delayed cortical myelination. Lineage-specific RNA-seq revealed that the oligodendrocyte master regulator Sox10 was significantly reduced, as well as myelination effectors, indicating impaired oligodendrocyte maturation. Chromatin immunoprecipitation assays of the same lineage showed increased H3K27me3 at promoter-proximal regions of Sox10, consistent with loss of KDM6B-mediated de-repression. Temporally controlled Sox10 induction partially rescued myelination in Kdm6b-cKO mice. These findings define a KDM6B→SOX10 axis that licenses oligodendrocyte development and cortical myelination by removing repressive H3K27me3 and sustaining active chromatin, with implications for KDM6B-related neurodevelopmental disorders.

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The Fosl1-Kdm6b Axis Controls Skeletal Muscle Fibrosis by Regulating Histone H3K27me3 [HiCAR]

Project description:Skeletal muscle fibrosis, characterized by the replacement of functional muscle tissue with fibrotic scarring, leads to muscle function loss and potentially fatal respiratory failure, particularly in muscular dystrophy. The mechanisms driving muscle fibrosis is not yet fully understood. Our study utilized single-cell RNA-seq and single-nuclei ATAC-seq to analyze the transcriptome and chromatin accessibility of regenerating and dystrophic skeletal muscle, identifying a specific subset of fibro-adipogenic precursors (FAPs) enriched in dystrophic muscles, termed fibrotic FAPs. We further demonstrated that chronic inflammation upregulates Fosl1, an early response gene, which activates the expression of Kdm6b in fibrotic FAPs. Kdm6b, a histone demethylase, specifically removes the repressive histone H3K27me3 mark. Notably, targeting Kdm6b genetically and pharmacologically inhibits fibrotic di^erentiation in human and mouse FAPs in vitro and ameliorated muscle fibrosis in mouse models in vivo. Furthermore, constitutive activation of the Fosl1-Kdm6b pathway reduced H3K27me3 modification at critical fibrotic gene loci, leading to their transcriptional activation. Taken together, our findings reveal that chronic inflammation perpetuates the Fosl1-Kdm6b axis in FAPs, causing epigenomic reprogramming and altering the H3K27me3 landscape, which is essential for preventing fibrotic differentiation of FAPs and skeletal muscle fibrosis.

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Autism-associated mutations in Kdm6b affect its role as a chromatin regulator in brain development

Project description:The regulation of gene expression in the developing brain is coordinated by changes in chromatin regulation. Chromatin regulation involves the deposition and removal of molecular modifications on the histone proteins that give structure to and control the function of genomic DNA. The trimethylation of histone H3 at lysine 27 (H3K27me3) is a chromatin mark that recruits transcriptional repressors, silencing gene transcription. The JmjC family lysine demethylase KDM6B has been identified as an enzyme that removes H3K27me3, allowing for expression of genes critical for brain development. Genetic variants in human KDM6B have been found to be associated with intellectual disability and autism spectrum disorder (ASD); however, the molecular mechanisms by which these genetic variants affect KDM6B function remain unknown. We mapped these variants into the structure of KDM6B, and computationally assessed their likely effects on KDM6B protein function. To experimentally determine how ASD-associated sequence variants in KDM6B affect the function of this protein in cells, we generated ASD-associated mutations into a KDM6B expression construct and assessed their effects on the enzymatic function of this protein as well as its stability and nuclear localization. We found that several ASD-associated mutations occur in the H3K27me3 binding pocket of KDM6B and impair the ability of this enzyme to demethylate histones. In parallel, through RNA sequencing experiments in cerebellar granule neurons from mouse, we found that expression of the enzymatically active form but not the enzymatically dead form of KDM6B was sufficient to rescue synaptic gene expression following knockdown of endogenous KDM6B. Together, these findings elucidate a novel role of KDM6B in controlling gene expression in maturing neurons, and they expand our knowledge on how chromatin dysregulation can lead to neurodevelopmental disorders like ASD.

2025-05-14 | GSE267688 | GEO

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