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Hypoxia-induced priming of microglial inflammatory gene expression is associated with TLR4 signaling H3K4me3 enrichment

ABSTRACT: We analyzed genome-wide H3K4me3 enichment and performed RNAseq analyses in N9 microglia cells after hypoxia exposure

ORGANISM(S): Mus musculus

PROVIDER: GSE108770 | GEO | 2020/02/04

REPOSITORIES: GEO

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Hypoxia-induced priming of microglial inflammatory gene expression is associated with TLR4 signaling H3K4me3 enrichment

Project description:Hypoxia-induced priming of microglial inflammatory gene expression is associated with TLR4 signaling H3K4me3 enrichment

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Hypoxia induces histone clipping and H3K4me3 loss in neutrophil progenitors resulting in long-term impairment of neutrophil immunity

Project description:The long-term impact of systemic hypoxia resulting from Acute Respiratory Distress Syndrome (ARDS) on the function of short-lived innate immune cells is unclear. We show that patients 3-6 months after recovering from ARDS have persistently impaired circulating neutrophil effector functions and an increased susceptibility to secondary infections. These defects are linked to a widespread loss of the activating histone mark H3K4me3 in genes crucial for neutrophil activities. By studying healthy volunteers exposed to altitude-induced hypoxemia, we demonstrate that oxygen deprivation alone causes this long-term neutrophil reprogramming. Mechanistically, mouse models of systemic hypoxia reveal that persistent loss of H3K4me3 originates in proNeu and preNeu progenitors within the bone marrow and is linked to N-terminal histone 3 clipping, which removes the lysine residue for methylation. Thus, we present novel evidence that systemic hypoxia initiates a sustained maladaptive reprogramming of neutrophil immunity by triggering histone 3 clipping and H3K4me3 loss in neutrophil progenitors.

2025-09-22 | PXD065461 | Pride

Hypoxia induces histone clipping and H3K4me3 loss in neutrophil progenitors resulting in long-term impairment of neutrophil immunity

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Prior Hypoxia Exposure Enhances Murine Microglial Inflammatory Gene Expression <i>in vitro</i> Without Concomitant H3K4me3 Enrichment.

Project description: Not available

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Hypoxia induces histone clipping and H3K4me3 loss in neutrophil progenitors resulting in long-term impairment of neutrophil immunity

Project description:A deeper understanding of the processes that sustain long-term reprogramming of rapidly turned-over cells in humans can offer unprecedented therapeutic potential, especially for immune cells like neutrophils, given their short lifespan in circulation and importance in both acute and chronic diseases. Hypoxia is a hallmark of a plethora of disease states and significantly shapes neutrophil effector functions. However, its potential contribution to long-term neutrophil reprogramming remains largely unexplored. We have observed persistent perturbations in newly formed circulating neutrophils’ phenotype and function in patients 3-6 months following hospitalisation with acute respiratory distress syndrome (ARDS), where poor oxygenation takes place. These lasting changes are associated with widespread loss of H3K4me3 in genomic regions of relevance to neutrophil activities. Notably, the replication of these findings in healthy volunteers months following altitude induced hypoxaemia attributes a role to the oxygen deprivation as a driver for long-term neutrophil reprogramming. Mechanistically, mouse models of systemic hypoxia reveal deleterious outcomes for infection and show that persistent loss of H3K4me3 originates in proNeu and preNeu populations within the bone marrow and is linked to hypoxia-driven n terminal histone 3 clipping. Thus, we present novel evidence that acute adaptations to systemic hypoxia trigger central changes in newly formed neutrophil populations, resulting in long-term impairment of effector functions and placing hypoxia as a crucial orchestrator of sustained neutrophil reprogramming.

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Expression profile of primary mouse microglial cultures exposed to hypoxia

Project description:Primary microglial cultures from neonatal mice were exposed to hypoxia (1% O2, 6 h) and their global gene expression profile was analyzed. This data were used to described the Hypoxic Microglia Signature, genes that were up- or down-regulated by hypoxia in microglial cells in culture.

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H3K4me3 and H3K27me3 ChIP-seq profiling in MCF7 cell lines under hypoxia and reoxygenation

Project description:Purpose: Study hypoxia and reoxygenation induced changes in genome-wide H3K4me3 and H3K27me3 occupancy Methods: Using the MCF7 breast epithelial adenocarcinoma cell line as a model, we studied epigenomic reprogramming as a function of fluctuating oxygen tension. To this end, we combined chromatin-immunoprecipitation and deep-sequencing analysis to identify H3K4me3-marks and H3K27me3-marks in MCF7 cells subjected to changes in oxygenation (i.e. acute hypoxia, chronic hypoxia, reoxygenation). Results: H3K4me3 and H3K27me3-marks showed a rapid global increase at specific sites throughout the genome under hypoxia, both genic and inter-genic, that was partly restored upon reoxygenation. Conclusions: Our data show that oxygen availability dynamically regulates the epigenetic state of the genome.

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Epigenetic coordination of transcriptional and translational programs in hypoxia

Project description:<p>Adaptation to cellular stresses entails an incompletely understood coordination of transcriptional and post-transcriptional gene regulation. Here, we quantified hypoxia-dependent transcriptomes, epigenomes and translatomes in T47D breast cancer cells and H9 human embryonic stem cells. This revealed alterations in H3K4me3 associating with pervasive changes in transcription start site (TSS) selection leading to remodeling of 5’UTRs, which act as critical hubs regulating translation, and a concomitant reshaping of translational landscapes. Moreover, modulating H3K4me3 could both recapitulate and block a subset of hypoxia-induced TSS switching, defining a role for H3K4me3 in TSS selection, independently of HIF1-dependent transcriptional mechanisms. While TSS switching is coordinated with the integrated stress response (ISR) and mTOR-guided translational reprogramming, it also acts independently to regulate translation in hypoxia. These results demonstrate a previously unappreciated mechanism of translational regulation driven by epigenetic reprogramming of the 5’UTRome, which is orchestrated with other hypoxia-triggered adaptive mechanisms.</p>

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Histone H3K4me3 signal breadth reveals constitutive and hypoxia stress responsive endometrial functions linked to endometriosis

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ApoE4 Drives Microglial Lipid Dysregulation in Alzheimer’s Disease via Epigenetic Reprogramming of the AsxL1/LXRα–H3K4me3 Axis

Project description:Background The ε 4 allele of apolipoprotein E gene (ApoE) stands as the greatest genetic risk factor for late-onset Alzheimer’s disease (AD). Although microglia accumulating lipid droplets (LDAM) have been implicated in AD pathogenesis, the mechanistic link between ApoE4 and microglial lipid dysregulation remains elusive. Methods We employed a multi-omics approach, combining snRNA-seq and locus-specific epigenetic analysis, alongside microglia-specific gene manipulation in ApoE-targeted replacement (TR) mice. Primary microglia were challenged with cholesterol to simulate lipid overload conditions. Results In mid-life ApoE4-TR mice, microglia within the dentate gyrus developed pronounced lipid droplet accumulation, concurrent with impaired Aβ clearance and a pro-inflammatory shift. snRNA-seq unveiled a unique microglial cluster in ApoE4 mice, enriched for lipid-metabolism genes and marked by the pronounced downregulation of the hub gene AsxL1. Mechanistically, ApoE4 attenuated the AsxL1–LXRα interaction, leading to reduced H3K4me3 occupancy at promoters of lipid-efflux genes such as Abca1. Crucially, CRISPR-mediated, microglia-specific overexpression of AsxL1 restored H3K4me3 levels, normalized cholesterol efflux, and rescued Aβ phagocytic deficits in vivo. Conclusions Our findings define an epigenetic pathway whereby ApoE4 drives microglial dysfunction via the AsxL1–LXRα–H3K4me3 axis, fostering the LDAM phenotype. Enhancing AsxL1 function presents a promising therapeutic avenue for countering ApoE4-mediated pathogenesis in AD.

2026-02-16 | GSE319246 | GEO

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