Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE224208 | GEO | 2024/04/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Macrophage epigenetic memories of early life injury drive neonatal nociceptive priming. [ATAC-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 | GSE224207 | GEO

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

| PRJNA930319 | ENA

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

Fingerprinting of the hNGF P61R100E gene expression in rat Dorsal Root Ganglion detected by microarray analysis

Project description:Nerve Growth Factor (NGF) is being considered as a therapeutic candidate for Alzheimer's disease (AD) treatment, not merely as a long-lasting cholinergic maintainer and neuroprotective agent but also as a direct anti-amyloidogenic factor. However, the development of a NGF-based therapy for neurodegenerative diseases is limited by the partial access of NGF to the brain and to its potent nociceptive actions in animals and humans. Indeed, NGF is involved in pain transmission and perception. The nociceptive activity of NGF is mediated through the activation of TrkA and p75NTR receptors on sensory nerve endings. Our group recently studied forms of NGF, mutated at residue R100, inspired by the human genetic disease HSAN V (Hereditary Sensory Autonomic Neuropathy Type V), which would allow increasing the dose of NGF without triggering pain. This “painless” hNGF hNGFP61S/R100E displays full neurotrophic and anti-amyloidogenic activities in neuronal cultures, and a reduced nociceptive activity in vivo, via a selective alteration of TrkA versus p75NTR binding and signaling. The molecular mechanism through which pNGF reduces nociceptive activity has never been investigated, therefore we performed gene expression microarray analysis to investigated the effect of hNGF hNGFP61S/R100E delivery in rat Dorsal Root Ganglia.

2017-04-18 | GSE80257 | 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

RRBS-based blood methylome in chronic nociceptive (NOCI) and neuropathic (NEURO) pain suffering patients and controls (CTL).

Project description:Nociceptive pain implies the activation of the nociceptors without damage to the somatosensory nervous system. Neuropathic pain implies an injury or a disease of the central or peripheral nervous system. Epigenomic may participate in chronic pain conditions as well as in the transition from acute to chronic pain. The purpose of the present study is to analyze how blood methylome differs in both mentionned types of chronic pain, by comparing them together and to controls. The study protocol was approved by the local ethic committee (CCVEM 034/12) and was conducted according to the recommendation of the Declaration of Helsinki. Patients were enrolled at the Clinique romande de réadaptation (CRR) in Sion, in Switzerland. Data were hosted and analyzed at the University of Geneva, Faculty of Medicine, Department of Genetic Medicine and Development, in Switzerland. Data were processed in the high performance computing cluster (HPC) nammed "Baobab" in the Geneva University.

2021-09-13 | GSE166255 | GEO

Transcription profiling of rat Postnatal developmental changes in Sprague-Dawley animals in the model of neuropathic pain - spare nerve injury

Project description:Neuropathic pain is an apparently spontaneous experience triggered by abnormal physiology of the peripheral or central nervous system, which evolves with time. Neuropathic pain arising from peripheral nerve injury is characterized by a combination of spontaneous pain, hyperalgesia and allodynia. There is no evidence of this type of pain in human infants or rat pups; brachial plexus avulsion, which causes intense neuropathic pain in adults, is not painful when the injury is sustained at birth. Since infants are capable of nociception from before birth and display both acute and chronic inflammatory pain behaviour from an early neonatal age, it appears that the mechanisms underlying neuropathic pain are differentially regulated over a prolonged postnatal period. We used microarrays to detail the global programme of gene expression underlying the differences in nerve injury between along the postnatal development and identified distinct classes of regulated genes during the injury Experiment Overall Design: We have performed a microarray analysis of the rat L4/L5 dorsal root ganglia, 7 days post spared nerve injury, a model of neuropathic pain. Genes that are regulated in adult rats displaying neuropathic behaviour were compared to those regulated in young rats (10 days old) that did not show the same neuropathic behaviour.

2010-01-30 | E-GEOD-15041 | biostudies-arrayexpress

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data