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Genome-wide maps of H3K4Me3 histone modification in human pulmonary endothelial cells under hypoxia

ABSTRACT: Genome-wide maps of H3K4Me3 histone modification in human pulmonary endothelial cells under hypoxia

PROVIDER: PRJNA789398 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17244535.fastq.gz	Fastqsanger.gz
	SRR17244536.fastq.gz	Fastqsanger.gz
	SRR17244537.fastq.gz	Fastqsanger.gz
	SRR17244538.fastq.gz	Fastqsanger.gz
	SRR17244539.fastq.gz	Fastqsanger.gz

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Genome-wide maps of H3K4Me3 histone modification in human pulmonary endothelial cells under hypoxia

Project description:Purpose: In lung tissue of mice with experimental PH, we identified an upregulated lncRNA 5031425E22 which mapped to a human ortholog KMT2E-AS1. Across mammals, this lncRNA gene sits adjacent (head-to-head) to the chromosomal location of the histone lysine N-methyltransferase 2E gene (KMT2E), a member of a family of regulators controlling histone 3 lysine 4 trimethylation (H3K4Me3) and chromatin remodeling. We found that both mouse lncRNA E22 and human KMT2E-AS1 were increased in multiple in vivo rodent and human instances of PH. This ChIP-sequencing study was designed to compare the histone 3 lysine 4 methylated regions/gene profile of human pulmonary arterial endothelial cells (HPAECs) under hypoxia as compared to normoxia. Method: Primary HPAECs were grown in EBM-2 basal medium supplemented with EGM-2 MV BulletKit (Lonza). Experiments were performed at passages 5 to 8. Cultured HPAECs were either under normoxia or hypoxia (0.2% oxygen) for 24 hours. Cells were fixed, crosslinked, and sonicated to get soluble chromatin for immunoprecipitation. 10% input of crosslinked DNA was saved while the remining DNA was precipitated with histone 3 lysine 4 antibody (H3K4Me3, Abcam, ab8580) or non-immune rabbit IgG (Pierce magnetic ChIP kit). Chromatin/antibody complex was then pulled down using Protein A/G Magnetic Beads (Pierece). DNA samples were proceeded with ChIP-sequencing (sequencing platform: DNBSeqTM, 20M reads).

2023-11-09 | GSE191027 | GEO

Hypoxia Induced Pulmonary Hypertension

Project description:Here we investigated the protein composition of the main pulmonary artery (MPA), distal pulmonary arteries (DPA) distal whole lung (DWL) of early stage hypoxia (using a neonatal bovine calf model) and late stage hypoxia (using adult steers with hypoxia-induced PH) using high resolution mass spectrometry. Compartment-resolved analysis allowed for quantitative measurements of proteins from cellular, soluble ECM and insoluble ECM fractions

2022-10-06 | MSV000090482 | MassIVE

Genome-wide maps of histone modification H3K4me3 in Daudi cells.

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Genome wide maps of H3K4me3 and H3ac histone modifications in C6 rat glioma cells [Illumina]

Project description:We report maps of H3K4me3 and H3ac - activiting expression histone modifications in C6 rat glioma cells. The data was obtained using whole genome high throughput technology. The sequencing was performed on HiSeq Ilumina platform. Examination of H3K4me3 histone modification and H3ac histone modification in C6 rat glioma cell line

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GNPS_2017 Mouse intermittent hypoxia (IH) - Aorta & pulmonary artery

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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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Physiological shear stress markedly alters the proteomic response to hypoxia in human pulmonary microvascular endothelial cells

Project description:Physiological shear stress, produced by blood flow, homeostatically regulates the phenotype of pulmonary endothelial cells exerting anti-inflammatory and anti-thrombotic actions and maintaining normal barrier function. In the pulmonary circulation hypoxia, due to high altitude or diseases such as COPD, causes vasoconstriction, increased vascular resistance and pulmonary hypertension. Hypoxia-induced changes in endothelial function play a central role in the development of this pulmonary hypertension. However, the direct interactive effects of hypoxia and shear stress on the pulmonary endothelial phenotype have not been extensively studied. We cultured human pulmonary microvascular endothelial cells (HPMEC) in normoxia or hypoxia while subjected to physiological shear stress or in static conditions. Unbiased proteomics was used to identify hypoxia-induced changes in protein expression. Using publicly available single cell RNA-seq datasets, differences in gene expression between the alveolar endothelial cells from COPD and healthy lungs were identified. 60 proteins were identified in HPMEC lysates whose expression changed in response to hypoxia in sheared but not in static conditions. mRNA for five of these (ERG, MCRIP1, EIF4A2, HSP90AA1 and DNAJA1) showed similar changes in the endothelial cells of COPD compared to healthy lungs. These data show that the proteomic responses of the pulmonary microvascular endothelium to hypoxia are significantly altered by shear stress and suggest that these differences are important in the development of hypoxic pulmonary vascular disease.

2023-02-17 | PXD036260 | Pride

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.

2025-09-22 | PXD065562 | Pride

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