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

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

PROVIDER: PRJNA1134737 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29789876_1.fastq.gz	Fastqsanger.gz
	SRR29789876_2.fastq.gz	Fastqsanger.gz
	SRR29789877_1.fastq.gz	Fastqsanger.gz
	SRR29789877_2.fastq.gz	Fastqsanger.gz
	SRR29789878_1.fastq.gz	Fastqsanger.gz

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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

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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 exposure induces epigenomic and transcriptomic-mediated preconditioning resembling epilepsy-associated microglial states.

Project description:Microglia play a crucial role in a range of neuropathologies through exacerbated activation. Microglial inflammatory responses can be influenced by prior exposures to noxious stimuli, like increased levels of extracellular adenosine and ATP. These are characteristic of brain insults like epileptic seizures and could potentially shape subsequent responses through epigenetic regulation. We investigated DNA methylation and expression changes in human microglia-like cells differentiated from monocytes following ATP-mediated preconditioning. We demonstrate that microglia-like cells display homeostatic microglial features, shown by surface markers, transcriptome, and DNA methylome. After exposure to ATP, TLR-mediated activation leads to an exacerbated pro-inflammatory response. These changes are accompanied by methylation and transcriptional reprogramming associated with enhanced immune-related functions. The reprogramming associated with ATP-mediated preconditioning leads to profiles found in microglial subsets linked to epilepsy. Purine-driven microglia immune preconditioning drives epigenetic and transcriptional changes that could contribute to altered functions of microglia during seizure development and progression.

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

Project description:DNA methylation profiling of monocytes and monocyte-derived microglia like cells. Innate immune memory was explored in microglia-like cells through consecutive exposure to ATP and LPS.The Illumina Infinium MethylationEPIC Beadchip was used to obtain DNA methylation profiles across approximately 850,000 CpGs.

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Single-cell RNA sequencing reveals distinct transcriptional features of the purinergic signaling in mouse trigeminal ganglion

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Project description:Stress preconditioning occurs when transient, sublethal stress events impact an organism's ability to counter future stresses. Although preconditioning effects are often noted in the literature, very little is known about the underlying mechanisms. To model preconditioning, we exposed a panel of genetically diverse Drosophila melanogaster to a sublethal heat shock and measured how well the flies survived exposure to endoplasmic reticulum (ER) stress. To identify genes with expression patterns predictive of preconditioning outcomes, we focused on the 10 DGRP strains at the extreme ends of our preconditioning screen. We compared the beneficial strains (RAL69, RAL93, RAL359, RAL387, RAL409) to the detrimental (RAL195, RAL304, RAL335, RAL737, RAL819) with and without heat shock (our preconditioning stress).

2023-04-25 | GSE226958 | GEO

Brain cell-specific origin of circulating microRNA biomarkers in experimental temporal lobe epilepsy

Project description:The diagnosis of epilepsy is complex and challenging and would benefit from the availability of molecular biomarkers, ideally measurable in a biofluid such as blood. Experimental and human epilepsy are associated with altered brain and blood levels of various microRNAs (miRNAs). Evidence is lacking, however, as to whether any of the circulating pool of miRNAs originates from the brain. To explore the link between circulating miRNAs and the pathophysiology of epilepsy, we first sequenced Ago2-bound miRNAs in plasma samples collected from mice subject to status epilepticus (SE) induced by intraamygdala microinjection of kainic acid. This identified time-dependent changes in plasma levels of miRNAs with known neuronal and microglial-cell origins. To explore whether the circulating miRNAs had originated from the brain, we generated mice expressing FLAG-Ago2 in neurons or microglia using tamoxifen-inducible Thy1 or Cx3cr1 promoters, respectively. FLAG immunoprecipitates from the plasma of these mice after seizures contained miRNAs, including let-7i-5p and miR-19b-3p. Taken together, these studies confirm that a portion of the circulating pool of miRNAs in experimental epilepsy originates from the brain, increasing support for miRNAs as mechanistic biomarkers of epilepsy.

2023-09-13 | GSE233890 | GEO

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