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Macrophage epigenetic memories of early life injury drive neonatal nociceptive priming. [RNA-Seq]

ABSTRACT: Macrophage epigenetic memories of early life injury drive neonatal nociceptive priming. [RNA-Seq]

PROVIDER: PRJNA930319 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23300800_1.fastq.gz	Fastqsanger.gz
	SRR23300800_2.fastq.gz	Fastqsanger.gz
	SRR23300801_1.fastq.gz	Fastqsanger.gz
	SRR23300801_2.fastq.gz	Fastqsanger.gz
	SRR23300802_1.fastq.gz	Fastqsanger.gz

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Macrophage epigenetic memories of early life injury drive neonatal nociceptive priming.

Project description:Macrophage epigenetic memories of early life injury drive neonatal nociceptive priming.

| PRJNA930315 | ENA

Macrophage epigenetic memories of early life injury drive neonatal nociceptive priming. [RNA-Seq]

Project description:The developing peripheral nervous and immune systems are functionally distinct from adults. These systems are vulnerable to effects of early life injury which can influence outcomes related to nociception following subsequent injury later in life (i.e. “neonatal nociceptive priming”). The underpinnings of this phenomenon are largely unknown, although critical periods in macrophages can be epigenetically trained by injury. We found that macrophages are both necessary and partially sufficient to drive neonatal nociceptive priming possibly due to a long-lasting epigenetic remodeling of peripheral macrophages. The p75 neurotrophic factor receptor (NTR) was found to be an important effector in regulating this “nociceptive trained immunity”. p75NTR modulates the inflammatory profile and responses of rodent and human macrophages and this “pain memory” was able to be transferred to a naive host to alter sex-specific pain-related behaviors. This study reveals a novel mechanism by which acute post-surgical pain may transition to chronic pain in children.

2024-04-22 | GSE224208 | GEO

Macrophage epigenetic memories of early life injury drive neonatal nociceptive priming. [ATAC-Seq]

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Macrophage epigenetic memories of early life injury drive neonatal nociceptive priming. [ATAC-Seq]

Project description:Macrophage epigenetic memories of early life injury drive neonatal nociceptive priming. [ATAC-Seq]

| PRJNA930318 | ENA

Macrophage epigenetic memories of early life injury drive neonatal nociceptive priming.

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

2024-04-22 | GSE224209 | GEO

Epigenetic priming of memory updating during reconsolidation to attenuate remote fear memories

Project description:Remembrances of traumata range among the most enduring forms of memories. Despite the elevated lifetime prevalence of anxiety disorders, effective strategies to attenuate long-term traumatic memories are scarce. The most efficacious treatments to diminish recent (i.e., day-old) traumata capitalize on memory updating mechanisms during reconsolidation that are initiated upon memory recall. Here, we show that in mice successful reconsolidation-updating paradigms for recent memories fail to attenuate remote (i.e., month-old) ones. We find that whereas recent memory recall induces a limited period of hippocampal neuroplasticity mediated, in part, by S-nitrosylation of HDAC2 and histone acetylation, such plasticity is absent for remote memories. However, by using an HDAC2-targeting inhibitor (HDACi) during reconsolidation, even remote memories can be persistently attenuated. This intervention epigenetically primes the expression of neuroplasticity-related genes as revealed by whole genome RNA sequencing, which is accompanied by higher metabolic, synaptic and structural plasticity. Thus, applying HDACis during memory reconsolidation might constitute a treatment option for remote traumata. 3 biological replicates per group were analyzed. The material analyzed was whole hippocampi from one brain hemisphere, from which total RNA was extracted.

2014-01-04 | E-GEOD-53794 | biostudies-arrayexpress

Epigenetic priming of memory updating during reconsolidation to attenuate remote fear memories

2014-01-04 | GSE53794 | GEO

Single-nucleus characterization of spinal dynorphin-lineage cells and identification of persistent transcriptional effects of neonatal hindpaw incision

Project description:Neonatal tissue damage can have long-lasting effects on nociceptive processing in the central nervous system, which may be partially due to persistent injury-evoked alteration of the normal balance between synaptic inhibition and excitation in the spinal dorsal horn. Spinal dynorphin-lineage (pDyn) neurons are part of an inhibitory circuit which limits the flow of nociceptive input from the periphery to the brain and is disrupted by neonatal tissue damage. To identify the potential molecular underpinnings of this disruption, an unbiased single-nucleus RNAseq analysis of adult spinal pDyn cells characterized this population in depth, then identified changes in gene expression evoked by neonatal hindpaw incision. The analysis revealed twelve transcriptionally distinct subpopulations (i.e., clusters) of dynorphin-lineage cells, including both inhibitory and excitatory neurons as well as oligodendrocytes and astrocytes. Investigation of injury-evoked differential gene expression identified genes which were significantly up- or downregulated in adult pDyn neurons from neonatally incised mice compared to naïve littermate controls. Some of these injury-evoked changes appeared to be cluster-specific while others were similar across all pDyn neuron clusters, and many of the identified genes were related to the cellular stress response. However, the relatively low number of injury-evoked differentially expressed genes also suggests that post-transcriptional regulation within pDyn neurons may play a key role in the priming of developing nociceptive circuits by early life injury. Overall, the findings reveal novel insight into the molecular heterogeneity of a key population of dorsal horn interneurons that has previously been implicated in the suppression of mechanical pain and itch.

2020-08-01 | GSE149527 | GEO

Nociceptive nerves regulate haematopoietic stem cell mobilization

Project description:Nociceptive neuropeptide CGRP acts directly on HSCs via the its receptor RAMP1/CALCRL, to promote egress by activating Gαs/Adenylyl cyclase/cAMP pathway.

2020-10-12 | GSE156449 | GEO

Effect of nociceptive neuropeptides on dendritic cells

Project description:We compared the effects of nociceptive neuropeptides and nociceptors on DCs by means of coculture of Flt3L-induced bone marrow-derived DCs and primary mouse nociceptors.

2023-04-01 | GSE217502 | GEO

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