Ontology highlight
ABSTRACT:
PROVIDER: PRJNA558152 | ENA |
REPOSITORIES: ENA
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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
Project description:This program addresses the gene signature associated with DRG in the Chung rat model for neuropathic pain. The Chung neuropathic pain profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in DRG of the Sprague Dawley rats following spinal nerve ligation compared to the sham-operated controls.
2013-03-22 | E-GEOD-38038 | biostudies-arrayexpress
Project description:Peripheral nerve injury alters the expression of hundreds of proteins in dorsal root ganglia (DRG). Targeting some of these proteins has led to successful treatments for acute pain, but not for sustained postoperative neuropathic pain. The latter may require targeting multiple proteins. Since a single microRNA (miR) can affect the expression of multiple proteins, here, we describe an approach to identify chronic neuropathic pain-relevant miRs. We used two variants of the spared nerve injury (SNI): Sural-SNI and Tibial-SNI and found distinct pain phenotypes between the two. Both models induced strong mechanical allodynia, but only Sural-SNI rats maintained strong mechanical and cold allodynia, as previously reported. In contrast, we found that Tibial-SNI rats recovered from mechanical allodynia and never developed cold allodynia. Since both models involve nerve injury, we increased the probability of identifying differentially regulated miRs that correlated with the quality and magnitude of neuropathic pain and decreased the probability of detecting miRs that are solely involved in neuronal regeneration. We found seven such miRs in L3-L5 DRG. The expression of these miRs increased in Tibial-SNI. These miRs displayed a lower level of expression in Sural-SNI, with four having levels lower than those in sham animals. Bioinformatics analysis of how these miRs could affect the expression of some ion channels supports the view that, following a peripheral nerve injury, the increase of the 7 miRs may contribute to the recovery from neuropathic pain while the decrease of four of them may contribute to the development of chronic neuropathic pain. The approach used resulted in the identification of a small number of potentially neuropathic pain relevant miRs. Additional studies are required to investigate whether manipulating the expression of the identified miRs in primary sensory neurons can prevent or ameliorate chronic neuropathic pain following peripheral nerve injuries. To identify the miRs that were differentially dysregulated between Tibial-SNI and Sural-SNI, we first performed 12 microarrays in a limited number of samples (in four individual DRGs per group: Sham, Tibial-SNI and Sural-SNI; two L3-DRG and two L4-DRG). Then, miRs identified as having differential expression were corroborated with real time qRT-PCR in RNA isolated from individual DRGs (L3, L4 and L5) derived from 4 rats per group (not presented here, but in the manuscript).
2014-09-29 | E-GEOD-60033 | biostudies-arrayexpress
Project description:To investigate mechanisms underlying neuropathic pain, we established sciatic nerve chronic constriction injury (CCI) neuropathic pain model in rats, and performed RNA-seq on ipsilateral bulk L4-L6 dorsal root ganglia from CCI rats and sham rats 11 days after surgery. By comprehensive analysis, we identified several key mRNAs and miRNAs, especially those associated with inflammatory immune response, may serve as promising targets, facilitating further investigation and eventually developing better therapeutic strategies for NP.
2023-03-15 | GSE212311 | GEO
Project description:Neuropathic pain is a troublesome pathological condition without suitable treatments. In this study, we performed RNA sequencing (RNA-seq) analysis to reveal transcriptomic profiles of spinal cord from chronic constriction injury (CCI) rats.
2022-04-05 | GSE175760 | GEO
Project description:Neuropathic pain (NP) is a complex, chronic pain condition caused by injury or dysfunction affecting the somatosensory nervous system. This study aimed to identify crucial miRNA in prelimbic cortex (PL) involved in NP rats. miRNA microarrays were applied in the present study.
2020-02-13 | GSE145199 | GEO
Project description:Neuropathic pain is a troublesome pathological condition without suitable treatments. In this study, we performed RNA sequencing (RNA-seq) analysis to reveal transcriptomic profiles of Anterior Cingulate Cortex (ACC) from chronic constriction injury (CCI) rats. We found 1628 differentially expressed genes (DEGs) were mainly involved in the inflammatory and immune process. Besides, cytokine signaling and other cell-defense related pathways mainly contribute to the occurrence and development of neuropathic pain. Then we classified the DEGs based on the time trend. Our results suggested that chemokines played a vital role in pain, and moreover, CCL5, CXCL9 and CXCL13, compared with CCL2, CCL3, CCL4, CCL6 and CCL7 had different time-dependent manners. In a word, targeting chemokines is of great significance to explore specific mechanisms and develop suitable drugs for neuropathic pain.
2022-04-05 | GSE172133 | GEO
Project description:Clinical observations indicate that vitamin D is a pain alleviating molecule. In order to unveil the molecular mechanisms at play, we performed an experimental study on rats with a neuropathic pain. After three weeks of vitamin D treatment, the cerebrum, the spinal cord and the dorsal root ganglia were collected for a transcriptomic analysis, using cDNA microarrays.
2018-04-29 | E-MTAB-6801 | biostudies-arrayexpress
Project description:Beta-endorphinergic neurons in the hypothalamic arcuate nucleus (ARC) synthesize beta-endorphin (β-EP) to alleviate nociceptive behaviors, although the underlying regulatory mechanisms remain unknown. Here, we elucidated a novel epigenetic pathway driven by microRNA regulation of beta-endorphin synthesis in ARC neurons to control neuropathic pain. In pain-injured rats miR-203a-3p was the most highly upregulated miRNA in the ARC. A similar increase was identified in the cerebrospinal fluid of trigeminal neuralgia patients. Mechanistically, histone deacetylase 9 downregulation increased acetylation of histone H3 lysine-18, facilitating the binding of NR4A2 transcription factor to the miR-203a-3p gene promoter increasing miR-203a-3p expression following nerve injury. Further, increased miR-203a-3p was found to maintain neuropathic pain by targeting proprotein convertase 1, an endopeptidase necessary for the cleavage of proopiomelanocortin, the precursor of β-EP. Our findings highlight an epigenetic regulatory pathway for β-EP synthesis that contributes to neuropathic pain development and maintenance mechanisms providing for new therapeutic targets for neuropathic pain treatment.
2023-10-17 | GSE216965 | GEO