Sex-specific transcriptome of spinal microglia in neuropathic pain due to peripheral nerve injury
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ABSTRACT:
PROVIDER: PRJNA748992 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15215600_1.fastq.gz | Fastqsanger.gz | |||
| SRR15215600_2.fastq.gz | Fastqsanger.gz | |||
| SRR15215601_1.fastq.gz | Fastqsanger.gz | |||
| SRR15215601_2.fastq.gz | Fastqsanger.gz | |||
| SRR15215602_1.fastq.gz | Fastqsanger.gz |
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Project description:Neuropathic pain is a prevalent and debilitating chronic disease that is characterized by activation in glial cells in various pain-related regions within the central nervous system. Recent studies have suggested a sexually dimorphic role of microglia in the maintenance of neuropathic pain in rodents. Here, we utilized RNA sequencing analysis of microglia to identify whether there is a common neuropathic microglial signature and characterize the sex differences in microglia in pain-related regions in nerve injury and chemotherapy-induced peripheral neuropathy mouse models. Whilst mechanical allodynia and behavioral changes were observed in all models, transcriptomic analysis of microglia revealed no common transcriptional changes in spinal and supraspinal regions and in different neuropathic models. However, there was a substantial change in microglial gene expression within the ipsilateral lumbar spinal cord 7-days after chronic constriction injury (CCI) of the sciatic nerve. Both sexes upregulated genes associated with inflammation, phagosome, and lysosome activation, though males revealed a prominent global transcriptional shift not observed in female mice. This study demonstrates a lack of a common neuropathic microglial signature and indicates distinct sex differences in spinal microglia, suggesting they contribute to the sex-specific pain processing following nerve injury.
2021-07-27 | GSE180627 | 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:Expression profiling of L4 and L5 Dorsal Root Ganglion (DRG) in the spinal nerve ligation model of neuropathic pain. The goal of the study was to identify genes involved in neuropathic pain This series of samples comprises of contralateral and ipsilateral L4 and L5 DRG tissue collected 4 weeks after rats underwent a L5 spinal nerve ligation (SNL) or a sham operation with no L5 spinal nerve ligation. This defines 8 groups (i) contralateral L4 DRG from the sham cohort (n=5), (ii) ipsilateral L4 DRG from sham cohort (n=5), (iii) contralateral L4 DRG from SNL cohort (n=5), (iv) ipsilateral L4 DRG from the SNL chort (n=5), (v) contralateral L5 DRG from the sham cohort (n=5), (vi) ipsilateral L5 DRG from sham cohort (n=5), (vii) contralateral L5 DRG from SNL cohort (n=5), (viii) ipsilateral L5 DRG from the SNL cohort (n=5)
2011-10-17 | E-GEOD-24982 | biostudies-arrayexpress
Project description:Expression profiling of L4 and L5 Dorsal Root Ganglion (DRG) in the spinal nerve ligation model of neuropathic pain. The goal of the study was to identify genes involved in neuropathic pain
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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.
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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: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:Microglia activation contributes to the development of neuropathic pain. To identify changes of microglial gene expression during their activation after peripheral nerve injury, we employed microarray analysis of individually collected pools of 10 spinal microglia cells
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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.
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