Ontology highlight
ABSTRACT:
PROVIDER: PRJNA814329 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18301970.fastq.gz | Fastqsanger.gz | |||
| SRR18301971.fastq.gz | Fastqsanger.gz | |||
| SRR18301972_1.fastq.gz | Fastqsanger.gz | |||
| SRR18301972_2.fastq.gz | Fastqsanger.gz | |||
| SRR18301973.fastq.gz | Fastqsanger.gz |
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Project description:Nerve injury-induced changes in gene expression in primary sensory neurons, such as trigeminal ganglion (TG) neurons, play a critical role in the genesis of neuropathic pain. Therefore, understanding the molecular mechanisms underlying these changes in the TGs following peripheral nerve injury will enable us to develop a new avenue for managing trigeminal-mediated neuropathic pain. Studies have highlighted the involvement of miRNA-mediated modulation in a wide range of diseases, leading to the exploration of miRNA-based therapeutics as a potential treatment strategy. Here, in this RNA-seq database, we have found that microRNA-216a-3p (miR-216a-3p) and miR-32-5p (miR-32-5p), which are downregulated in injured TGs, are novel functional RNAs involved in regulating trigeminal-mediated neuropathic pain. Histone methylation-mediated miRNA downregulation in TG neurons regulates trigeminal neuropathic pain by targeting either STIM1 (H3K27me3/SOX10/miR-216a-3p/STIM1) or Cav3.2 (GR/miR-32-5p/Cav3.2) channels. Moreover, we found that miR-323-3p exhibited the most significant upregulation in the injured TG. Understanding the mechanistic role of the PRMT2/FOXA2/miR-323-3p/Kv2.1 signaling axis in sensory neurons may advance the discovery of novel therapeutic strategies for neuropathic pain.
2025-01-08 | GSE192803 | GEO
Project description:Trigeminal neuralgia (TN) is a type of neuropathic pain caused by injury to sensory nerves, manifesting as severe paroxysmal pain of the head and face. Trigeminal neuralgia brings a huge burden to patients, without long-term effective treatment. Changes in the expression of pain-related genes in the whole blood samples of patients play an important role in the pathogenesis, diagnosis, and evaluation of treatment effects of trigeminal neuralgia. To better understand the mechanism of trigeminal neuralgia, we collect the whole blood samples from the trigeminal neuralgia patients and the pain-free healthy comparisons. RNA-seq was conducted between the two groups to find the transcriptome changes in patients with trigeminal neuralgia.
2021-10-28 | GSE186505 | GEO
Project description:The cerebral cortex plays a key role in the multi-dimensional human pain experience. However, the neural mechanisms mediating pain-related cortical activity remain largely unknown, particularly in primary somatosensory cortex (S1). We therefore developed a new animal model of trigeminal neuralgia, a prototypical neuropathic pain, which allowed us to evaluate pain-related cortical dynamics with unprecedented translational relevance. Our novel model (FLIT: Foramen Lacerum Impingement of Trigeminal-nerve) displayed robust clinically relevant trigeminal neuralgia-like behaviors, including asymmetric facial grimacing, dental pain-like behaviors, anxiety-like behavior, and sexual dysfunction, capturing many features of the human pain experience. Awake FLIT mice exhibited highly synchronized spontaneous population activity in S1, due to GABAergic interneuron hypoactivity. Remarkably, clinically effective treatments including carbamazepine and trigeminal nerve root decompression abrogated S1 synchronization and alleviated trigeminal neuralgia-like behaviors. These results reveal synchronized S1 activity as a new and important cortical substrate of neuropathic pain, which can be clinically targeted to provide effective therapy.
2023-02-10 | GSE162284 | GEO
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
Project description:Although miRNA-mediated epigenetic regulation has been investigated as a potential therapeutic strategy for diseases, its exact functional regulatory contributions to neuropathic pain have not yet been fully elucidated. Herein, we revealed miR-323-3p as a key functional noncoding RNA in modulating trigeminal neuropathic pain. Through combined high-throughput sequencing and qPCR analysis, we revealed that miR-323-3p was most significantly upregulated in the injured trigeminal ganglion (TG). The administration of a miR-323-3p antagomir via intra-TG injection or blockade of miR-323-3p through lentiviral delivery specifically targeting neurons in injured TGs suppressed established trigeminal neuropathic pain. While miR-323-3p inhibition had no effect on inflammatory pain, local induction of miR-323-3p in naive TGs directly elicited pain hypersensitivity. Mechanistically, nerve injury caused upregulated protein expression of arginine methyltransferase 2 (PRMT2), which promotes asymmetric demethylation of H3R8 (H3R8me2a), thereby facilitating the binding of the forkhead box A2 (FOXA2) transcription factor to the miR-323-3p promoter and resulting in the upregulation of miR-323-3p expression. Furthermore, the increase in miR-323-3p expression induced significant reductions in Kv2.1 protein expression and channel currents, resulting in TG neuronal hyperexcitability. Conversely, downregulation of miR-323-3p in the injured TG reversed the decrease in Kv2.1 expression and attenuated nerve injury-induced mechanical allodynia. Thus, miR-323-3p upregulation is causally involved in the development of trigeminal neuropathic pain through the regulation of Kv2.1 channels in the TG. The mechanistic understanding of the PRMT2/FOXA2/miR-323-3p/Kv2.1 signaling axis in sensory neurons may enable the discovery of new therapeutic targets for neuropathic pain management.
2025-06-08 | GSE224814 | GEO
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:Pain sensing neurons, nociceptors, are key drivers of neuropathic pain. We used translating ribosome affinity purification (trap) to comprehensively characterize up- and down-regulated mRNA translation in Scn10a-positive nociceptors in chemotherapy-induced neuropathic pain. We provide evidence that an underlying mechanism driving these changes in gene expression is a sustained mTORC1 activation driven by MNK1-eIF4E signaling. RagA, a GTPase controlling mTORC1 activity, is identified as a novel target of MNK1-eIF4E signaling, demonstrating a new link between these distinct signaling pathways. Neuropathic pain and RagA translation are strongly attenuated by genetic ablation of eIF4E phosphorylation, MNK1 elimination or treatment with the MNK inhibitor eFT508. We reveal a novel translational circuit for the genesis of neuropathic pain with important implications for next generation neuropathic pain therapeutics.
2018-08-01 | GSE113941 | GEO
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
2009-12-18 | GSE15041 | GEO
Project description:Intractable neuropathic pain is recognized as a common symptom of neuromyelitis optica spectrum disorder (NMOSD). However, the underlying mechanism of NMOSD pain remains to be elucidated. Here, we established NMOSD pain model by injecting anti-AQP4 recombinant autoantibodies (AQP4-Ab) generated from NMOSD patient’s plasmablasts into rat spinal cords and confirmed the development of mechanical allodynia. AQP4-Ab mediated extracellular ATP release from astrocytes and pharmacological inhibition of ATP receptor reversed mechanical allodynia in NMOSD pain model. Furthermore, transcriptome analysis revealed microglia activation and IL-1β elevation in NMOSD spinal cord. Inhibition of microglia activation and neutralization of IL-1β also attenuated neuropathic pain in NMOSD rat model. In addition, the human CSF ATP concentration was significantly higher in the acute and remission phase of NMOSD than in multiple sclerosis and other neurological disorder patients. These findings indicate ATP, microglial activation and IL-1β secretion orchestrates the pathogenesis of NMOSD neuropathic pain.
2021-08-24 | GSE150598 | GEO
Project description:Neuropathic pain (NP), defined as a complex chronic pain state caused by somatosensory nervous system lesions or diseases, is currently the most challenging clinical neurological disorder in the world. The main signs and symptoms of NP include spontaneous pain, abnormal pain and hyperalgesia. It is generally believed that the specific pathological causes of NP include spinal cord or peripheral spinal cord injury, postherpetic neuralgia, trigeminal neuralgia, and tumor invasion. While the critical role of mRNA in NP is well recognized, the involvement of mRNA in the development of NP remains to be elucidated. Therefore, in this study, we explored changes in mRNA expression profiles through transcriptome sequencing to provide a landscape of mRNA dysregulation in the NP spinal cord.
2024-09-01 | GSE256472 | GEO