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

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

PROVIDER: PRJNA930315 | 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. [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.

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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]

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

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

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

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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.

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