Gene expression of spinal cord in neuropathic pain rats treated by paeoniflorin- liquiritin combination
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ABSTRACT:
PROVIDER: PRJNA848218 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19631200_1.fastq.gz | Fastqsanger.gz | |||
| SRR19631200_2.fastq.gz | Fastqsanger.gz | |||
| SRR19631201_1.fastq.gz | Fastqsanger.gz | |||
| SRR19631201_2.fastq.gz | Fastqsanger.gz | |||
| SRR19631202_1.fastq.gz | Fastqsanger.gz |
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Project description:To investigate the alleviating effect of paeoniflorin-liquiritin combination on neuropathic pain, we performed gene expression profiling analysis using data obtained from RNA-seq of spinal cord in spared nerve injury rats
2022-09-28 | GSE205906 | GEO
Project description:Astrocytes in the spinal cord dorsal horn (SDH) play a pivotal role in synaptic transmission and neuropathic pain. However, the precise classification of SDH astrocytes in health and disease remains elusive. Here we reveal Gpr37l1 as a marker and functional regulator of spinal astrocytes. Through single-nucleus RNA sequencing, we identified Gpr37l1 as a selective GPCR marker for spinal cord astrocytes. Notably, SDH displayed reactive astrocyte phenotypes and exacerbated neuropathic pain following nerve injury combined with Gpr37l1 deficiency. In naïve animals, GPR37L1 knockdown in SDH astrocytes induces astrogliosis and pain hypersensitivity, while Gpr37l1-/- mice fail to recover from neuropathic pain. GPR37L1 activation by maresin-1 increased astrocyte GLT-1 activity and reduced spinal EPSCs and neuropathic pain. Selective overexpression of Gpr37l1 in SDH astrocytes reversed neuropathic pain and astrogliosis after nerve injury. Our findings illuminate astrocyte GPR37l1 as an essential negative regulator of pain, which protects neuropathic pain through astrocyte signaling in SDH.
2025-02-14 | GSE286467 | GEO
Project description:Objective: Chronic pain is a major problem in patients with spinal cord injury (SCI). According to different studies, approximately 70% of patients with SCI experience persistent pain. Although previous gene expression profiling studies have been conducted in animal models, gene expression profiling study in human whole blood has not been reported yet. The objective of this study was to define the gene expression profile of neuropathic pain in spinal cord injured patients. Materials and Methods: We performed gene expression analysis including 20.000 genes using Affymetrix GeneChip® Primeview™ Human Gene Expression Arrays. For confirmation of expression levels of selected genes, we performed real time polymerase chain reaction. We gathered samples from periferic blood mononuclear cells. Data of twelve patients with intractable neuropathic pain was compared with thirteen patients who don’t have pain. All patients have complete injuries with a level of injury above T5. Results: A total of 16 differentially expressed genes including 9 up-regulated and 7 down-regulated were obtained with a cut-off degree at 4 fold change. EIF1AY, RPS4Y1, DDX3Y, RPL31, ETS1, KLF3, JUN, CYorf15B, and ERAP2 were in up-regulated and HLA-C, XIST, C4BPA, FAM118A, ZNF506, OVOS2, and C1D were in down-regulated group. KEGG pathway database showed that 14.6% of genes were enriched in the nodes of immune system. Real time polymerase chain reaction analyses did not increase to statistically significant levels for confirmation of gene expression analyze results. Conclusions: Considering these data, findings of this first gene expression study in humans with SCI might provide valuable information for future targets for understanding neuropathic pain pathogenesis. The results of gene expression analyses were not confirmed by real time polymerase chain reaction. Studies with larger sample size are needed for confirmation. This is a cross-sectional study with a control group. Patients were divided into two groups according to intractable neuropathic pain existence.There were 12 patients in group A (Patients with pain) and 13 patients in control group.
2015-06-16 | E-GEOD-69901 | biostudies-arrayexpress
Project description:We produced single-cell transcriptomes from the mouse spinal cord using Drop-seq in animals modeling neuropathic pain and superficial injury (SI) controls. We used the spared nerve injury (SNI) model of neuropathic pain. ~10,000 cells from sham surgery controls and ~9,000 cells from SNI animals were sequenced. Unbiased cell clustering yielded 66 spinal cell subtypes sequenced at relatively low depth (~1200 transcripts/cell). Comparisons between SI and SNI cells were performed to investigate cell-specific differences during a neuropathic pain state.
2021-03-04 | GSE134003 | GEO
Project description:Sensitization of spinal nociceptive circuits plays a cardinal role in neuropathic pain. This sensitization depends on new gene expression that is primarily regulated via transcriptional and translational control mechanisms. The relative roles of these mechanisms in regulating gene expression in the clinically relevant chronic phase of neuropathic pain are not well understood. Here, we show that changes in gene expression in the spinal cord during the chronic phase of neuropathic pain are substantially regulated at the translational level. Downregulating spinal translation at the chronic phase alleviated pain hypersensitivity. Cell-type-specific profiling revealed that spinal inhibitory neurons exhibited greater changes in translation after peripheral nerve injury compared to excitatory neurons. Notably, increasing translation selectively in all inhibitory neurons or parvalbumin-positive (PV + ) interneurons, but not excitatory neurons, promoted mechanical pain hypersensitivity. Furthermore, increasing translation in PV + neurons decreased their intrinsic excitability and spiking activity, whereas reducing translation in spinal PV + neurons prevented the nerve injury-induced decrease in excitability. Thus, translational control mechanisms in the spinal cord, primarily in inhibitory neurons, play a critical role in mediating neuropathic pain hypersensitivity.
2024-04-30 | GSE265957 | GEO
Project description:Histone deacetylase inhibitors (HDACIs) interfere with the epigenetic process of histone acetylation and are known to have analgesic properties in models of chronic inflammatory pain. The aim of this study was to determine whether these compounds could also affect neuropathic pain. Different class I HDACIs were delivered intrathecally into rat spinal cord in models of traumatic nerve injury and antiretroviral drug-induced peripheral neuropathy (stavudine, d4T). Mechanical and thermal hypersensitivity was attenuated by 40% to 50% as a result of HDACI treatment, but only if started before any insult. The drugs globally increased histone acetylation in the spinal cord, but appeared to have no measurable effects in relevant dorsal root ganglia in this treatment paradigm, suggesting that any potential mechanism should be sought in the central nervous system. Microarray analysis of dorsal cord RNA revealed the signature of the specific compound used (MS-275) and suggested that its main effect was mediated through HDAC1. Taken together, these data support a role for histone acetylation in the emergence of neuropathic pain. n = 4, HDACi treated vs. vehicle treated. Ipsilateral dorsal spinal cord tissue after L5 spinal nerve transection, DRG tissue was run in a separate Affymetrix experiment.
2013-10-01 | E-GEOD-51294 | biostudies-arrayexpress
Project description:Chronic pain arises from an imbalance between excitation and inhibition. For chronic pain caused by peripheral nerve injury, sensory neuron damage leads to changes in spinal pain transduction, where enhanced excitatory and/or loss of inhibitory pathways can drive pain diseases. At the cellular level, the transcriptional changes occurring in entrenched chronic pain are largely unknown. Here we use single nuclei and spatial transcriptomic approaches to investigate the cellular and molecular causes of entrenched and treated neuropathic pain. Our data show that nerve injury leads to broad upregulation of spinal synaptic and excitatory pathways in dorsal neuronal and glial populations. We confirm these core populations are conserved in the human spinal cord, and show an effective pain therapy acts by dampening these neuropathic transcriptional programs. Overall, our data provides the first high resolution transcriptional analysis of the neuropathic spinal cord, highlighting known and novel pathways that may help us better manage pain diseases.
2026-04-28 | GSE328700 | GEO
Project description:Chronic pain arises from an imbalance between excitation and inhibition. For chronic pain caused by peripheral nerve injury, sensory neuron damage leads to changes in spinal pain transduction, where enhanced excitatory and/or loss of inhibitory pathways can drive pain diseases. At the cellular level, the transcriptional changes occurring in entrenched chronic pain are largely unknown. Here we use single nuclei and spatial transcriptomic approaches to investigate the cellular and molecular causes of entrenched and treated neuropathic pain. Our data show that nerve injury leads to broad upregulation of spinal synaptic and excitatory pathways in dorsal neuronal and glial populations. We confirm these core populations are conserved in the human spinal cord, and show an effective pain therapy acts by dampening these neuropathic transcriptional programs. Overall, our data provides the first high resolution transcriptional analysis of the neuropathic spinal cord, highlighting known and novel pathways that may help us better manage pain diseases.
2026-04-28 | GSE325938 | GEO
Project description:Chronic pain arises from an imbalance between excitation and inhibition. For chronic pain caused by peripheral nerve injury, sensory neuron damage leads to changes in spinal pain transduction, where enhanced excitatory and/or loss of inhibitory pathways can drive pain diseases. At the cellular level, the transcriptional changes occurring in entrenched chronic pain are largely unknown. Here we use single nuclei and spatial transcriptomic approaches to investigate the cellular and molecular causes of entrenched and treated neuropathic pain. Our data show that nerve injury leads to broad upregulation of spinal synaptic and excitatory pathways in dorsal neuronal and glial populations. We confirm these core populations are conserved in the human spinal cord, and show an effective pain therapy acts by dampening these neuropathic transcriptional programs. Overall, our data provides the first high resolution transcriptional analysis of the neuropathic spinal cord, highlighting known and novel pathways that may help us better manage pain diseases.
2026-04-28 | GSE328175 | 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