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Epigenomic preconditioning of peripheral monocytes determines their transcriptional response to the tumor microenvironment

ABSTRACT: Epigenomic preconditioning of peripheral monocytes determines their transcriptional response to the tumor microenvironment

PROVIDER: PRJNA1119638 | ENA |

REPOSITORIES: ENA

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	SRR29271045_1.fastq.gz	Fastqsanger.gz
	SRR29271045_2.fastq.gz	Fastqsanger.gz
	SRR29271047_1.fastq.gz	Fastqsanger.gz
	SRR29271047_2.fastq.gz	Fastqsanger.gz

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Epigenomic preconditioning of peripheral monocytes determines their transcriptional response to the tumor microenvironment

Project description:Monocytes are recruited to tumors and undergo transcriptional reprogramming resulting in tumor-promoting functions. Epigenomic features, such as post-translational modification of histones and chromatin accessibility, are key determinants of transcription factor binding and thereby play an important role in determining transcriptional responses to the tissue environment. It remains unknown whether systemic tumor-associated signals could alter the epigenomic landscape of peripheral monocytes before they reach the tumor, thus shaping their subsequent response to the tumor microenvironment. Here, we performed genome-wide analyses of multiple histone modifications (H3K4me1, H3K4me3, H3K27ac) and chromatin accessibility in a mouse model and found that the distal tumor caused extensive remodeling of both H3K4me3+ promoters and H3K4me1+ enhancers in peripheral monocytes. Specifically, this involved the repression of interferon-responsive regulatory elements as well as the stablishment of enhancers harboring binding motifs for transcription factor families downstream of pro-inflammatory signaling, such as C/EBP, AP-1 and STAT. Reprogrammed enhancers in peripheral monocytes could be linked to sustained gene expression changes that persisted after tumor infiltration. In addition, key pro-tumor genes upregulated in tumor-infiltrating monocytes showed epigenetic priming already in the circulation. Overall, these results indicate that the epigenomic landscape of peripheral monocytes is altered in response to a distal tumor, and this can shape the transcriptional response of monocytes to the tumor microenvironment.

2025-06-25 | GSE268992 | GEO

Purinergic Preconditioning Induces Epigenomic and Transcriptomic Changes Resembling Epilepsy-associated Microglial States

Project description:Microglia are the main immune effector cells in the central nervous system (CNS) and contribute to a wide spectrum of neuropathological conditions through exacerbated activation. Microglial inflammatory responses may be conditioned by prior exposures to noxious stimuli, such as increased levels of extracellular adenosine and ATP. These levels are characteristic of brain insults like epileptic seizures and could potentially determine subsequent responses through epigenetic regulation. In this study, we investigated DNA methylation and expression changes in microglia-like cells differentiated from monocytes following ATP-mediated preconditioning. First, during microglia differentiation, we mainly observed DNA demethylation in genomic sequences enriched in binding motifs of microglia lineage transcription factors like PU.1, consistent with the relevance of this factor in in vivo microglia. TLR-mediated activation, after a first exposure to ATP, promoted exacerbated pro-inflammatory activation in comparison to cells not pre-exposed to ATP. These changes were accompanied by DNA methylation and transcriptional reprogramming of immune-related pathways, neurotransmitter activity and nucleotide phosphorylation. Finally, the epigenetic and transcriptional reprogramming associated with ATP-mediated preconditioning results in profiles found in microglia subsets linked to epilepsy. Purine-driven microglia immune pre-conditioning associates with epigenetic and transcriptional changes that might contribute to altered functions of microglia during seizure development and progression, particularly associated with neuroinflammation.

2024-07-11 | GSE272030 | GEO

Purinergic Preconditioning Induces Epigenomic and Transcriptomic Changes Resembling Epilepsy-associated Microglial States

Project description:Purinergic Preconditioning Induces Epigenomic and Transcriptomic Changes Resembling Epilepsy-associated Microglial States

| PRJNA984338 | ENA

Purinergic Preconditioning Induces Epigenomic and Transcriptomic Changes Resembling Epilepsy-associated Microglial States

Project description:Purinergic Preconditioning Induces Epigenomic and Transcriptomic Changes Resembling Epilepsy-associated Microglial States

| PRJNA1134737 | ENA

Genomics of preconditioning

Project description:Isolated perfused rat hearts exposed to isoflurane or ischemic preconditioning, a subgroup followed by 40 minutes of ischemia and 3 hours of reperfusion. Exact protocol available from the authors. Keywords = preconditioning Keywords = anesthetics Keywords = ischemia/reperfusion Keywords: other

2004-07-30 | GSE1616 | GEO

Bone marrow microenvironment: interaction of monocytes and stromal cells

Project description:Two human stromal cell lines, HS-5 and HS-27a, represent functionally distinct components of the bone marrow microenvironment. A third influential component of the microenvironment is resident monocytes and macrophages. The baseline expression profile of normal peripheral blood monocytes was determined and their effect on the gene expression of the stromal cells was investigated in a co-culture sytem. Control RNA for all samples was Stratagene Universal human reference RNA. Keywords: Cell Line Comparison and Culture Comparison

2005-10-25 | GSE3472 | GEO

Preconditioning Biochar-Fungal analyses

Project description:Preconditioning Biochar-Fungal analyses

| PRJNA415278 | ENA

Ezrin drives adaptation of monocytes to the inflamed lung microenvironment

Project description:Ezrin drives adaptation of monocytes to the inflamed lung microenvironment

| PRJNA1111746 | ENA

Transcription profiling by array of human bone marrow stromal cells lines cultured with monocytes to investigate interactions in the hematopoietic microenvironment

Project description:The hematopoietic microenvironment consists of non-hematopoietic derived stromal elements and hematopoietic derived monocytes and macrophages which interact and function together to control the proliferation and differentiation of early blood-forming cells. Two human stromal cell lines (HS-5 and HS-27a) representing distinct functional components of this microenvironment have been extensively characterized and shown to influence monocyte gene expression. This series of gene expression profiles is intended to extend the previous studies and identify which gene expression changes may require cell-cell contact or occur in the stromal cells as a result of monocyte influence;or in the monocytes as a result of stormal influences. Experiment Overall Design: Two human bone marrow stromal cell lines (HS5 and HS27a) were cultured with and without monocytes (CD14+ cells) from 2 different donors. Experiment Overall Design: culture condition: stroma no monocytes: HS5-1, HS5-2, HS27a-1, HS27a-2 Experiment Overall Design: culture condition: stroma with monocytes: HS5-MO-1, HS5-MO-2, HS27a-MO-1, HS27a-MO-2 Experiment Overall Design: donor: donor 3: HS5-MO-1, HS27a-MO-1 Experiment Overall Design: donor: donor 4: HS5-MO-2, HS27a-MO-2 Experiment Overall Design: cell line: HS5: HS5-1, HS5-2, HS5-MO-1, HS5-MO-2 Experiment Overall Design: cell line: HS27a: HS27a-1, HS27a-2, HS27a-MO-1, HS27a-MO-2

2008-04-07 | E-GEOD-10595 | biostudies-arrayexpress

Ezrin drives adaptation of monocytes to the inflamed lung microenvironment

Project description:Ezrin, an actin-binding protein, plays a crucial role in organizing the cellular cortical cytoskeleton and plasma membrane during cell migration, adhesion, and proliferation. While there is a good understanding of ezrin's function in cell types such as epithelial cells and lymphocytes, its role in monocytes/macrophages (MΦs) is less understood. Here, we used a monocyte/MΦ-specific ezrin knock-out mouse model to investigate the contribution of ezrin to monocyte recruitment and adaptation to the lung extracellular matrix (ECM) in response to lipopolysaccharide (LPS). Our study revealed that LPS induces ezrin expression in monocytes/MΦs, and that ezrin is essential for monocytes to adhere to lung ECM, proliferate, and differentiate into tissue-resident interstitial MΦs. Notably, ezrin is not required for monocyte extravasation into the lung parenchyma. Mechanistically, the loss of ezrin in monocytes disrupts activation of FAK and AKT signaling, which are necessary for lung-recruited monocytes and monocyte-derived MΦs to adhere to the ECM, proliferate, and survive. In summary, our data suggest that ezrin plays a role beyond structural cellular support, influencing diverse monocytes/MΦ processes and signaling pathways in response to infections, driving their adaptation to the lung microenvironment.

2024-11-07 | GSE267506 | GEO

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