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Regulatory T-cells inhibit microglia-induced pain hypersensitivity in female mice [exp2]

ABSTRACT: Regulatory T-cells inhibit microglia-induced pain hypersensitivity in female mice [exp2]

PROVIDER: PRJNA766541 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16081373.fastq.gz	Fastqsanger.gz
	SRR16081374.fastq.gz	Fastqsanger.gz
	SRR16081375.fastq.gz	Fastqsanger.gz
	SRR16081376.fastq.gz	Fastqsanger.gz
	SRR16081377.fastq.gz	Fastqsanger.gz

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Regulatory T-cells inhibit microglia-induced pain hypersensitivity in female mice

Project description:Regulatory T-cells inhibit microglia-induced pain hypersensitivity in female mice

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Regulatory T-cells inhibit microglia-induced pain hypersensitivity in female mice [exp1]

Project description:Regulatory T-cells inhibit microglia-induced pain hypersensitivity in female mice [exp1]

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Regulatory T-cells inhibit microglia-induced pain hypersensitivity in female mice [exp2]

Project description:RNA-sequencing data of female lumbar dorsal horn spinal cord microglia from WT or Treg KO mice after 3 days of CSF1 i.t. injection.

2021-09-27 | GSE184800 | GEO

4E-BP1-dependent translation in microglia controls mechanical hypersensitivity

Project description:Spinal microglia play a pivotal role in the development of neuropathic pain. Peripheral nerve injury induces changes in the transcriptional profile of microglia, including increased expression of components of translational machinery. Whether microglial protein synthesis is stimulated following nerve injury and has a functional role in mediating pain hypersensitivity is unknown. Here, we show that nascent protein synthesis is upregulated in spinal microglia following peripheral nerve injury. Stimulating mRNA translation in microglia, via selective ablation of the translational repressor, eukaryotic initiation factor 4E-binding protein 1 (4E-BP1), promoted the transition of microglia to a reactive state and induced mechanical hypersensitivity. Conversely, inhibiting microglial translation by expressing mutant 4E-BP1 in microglia attenuated their peripheral nerve injury-induced activation and alleviated neuropathic pain. Thus, the stimulation of 4E-BP1-dependent translation promotes microglia reactivity and mechanical hypersensitivity, whereas its inhibition alleviates neuropathic pain.

2024-01-31 | GSE254472 | GEO

4E-BP1-dependent translation in microglia controls mechanical hypersensitivity

Project description:Spinal microglia play a pivotal role in the development of neuropathic pain. Peripheral nerve injury induces changes in the transcriptional profile of microglia, including increased expression of components of translational machinery. Whether microglial protein synthesis is stimulated following nerve injury and has a functional role in mediating pain hypersensitivity is unknown. Here, we show that nascent protein synthesis is upregulated in spinal microglia following peripheral nerve injury in both male and female mice. Stimulating mRNA translation in microglia, by selectively ablating the translational repressor eukaryotic initiation factor 4E-binding protein 1 (4E-BP1), promoted the transition of microglia to a reactive state and induced mechanical hypersensitivity in both sexes, whereas spontaneous pain was increased only in males. Conversely, inhibiting microglial translation by expressing a mutant form of 4E-BP1 in microglia attenuated their activation following peripheral nerve injury and alleviated neuropathic pain in both sexes. Thus, stimulating 4E-BP1-dependent translation promotes microglial reactivity and mechanical hypersensitivity, whereas inhibiting it alleviates neuropathic pain.

2025-02-25 | GSE285677 | GEO

The circadian clock component REV-ERBs is an analgesic target for cancer-induced tactile pain hypersensitivity

Project description:Neuropathic pain is one of the most intractable pain conditions associated with tumor growth compressing and damaging nerves. A troublesome hallmark symptom of neuropathic pain is hypersensitivity to innocuous stimuli, known as “tactile allodynia,” which is often refractory to currently available analgesics. Diurnal variations in pain hypersensitivity are common in patients with cancer, but the underlying mechanisms are enigmatic. Herein, we report that spinal expression of lipocalin-2 (LCN2) enhances pain sensitivity of NCTC2472 fibrosarcoma-implanted male mice during specific stages of the diurnal cycle. As the tumor grew, interleukin-6 (IL-6) levels increased in the spinal cord of the mice. Increased IL-6 levels stimulated LCN2 expression in spinal microglia, but this expression was periodically repressed by the circadian clock components REV-ERBα and REV-ERBβ. Notably, intra-spinal dorsal horn injection of lentiviral vectors expressing REV-ERBα or REV-ERBβ in tumor-bearing mice alleviated tactile allodynia. Furthermore, intrathecal injection of SR9009, a synthetic agonist of REV-ERBs, also attenuated cancer-induced pain hypersensitivity, accompanied by suppressing spinal LCN2 expression. These results suggest that temporal elevation of LCN2 expression decreases the threshold of tactile pain hypersensitivity induced by tumor growth. We propose that the circadian clock component of REV-ERBs is an effective target for alleviation of cancer-induced tactile allodynia, identifying a new class of analgesic agents.

2025-04-27 | GSE255355 | GEO

Regulatory T-cells inhibit microglia-induced pain hypersensitivity in female mice [exp1]

Project description:RNA-sequencing data of male and female lumbar dorsal horn spinal cord microglia after 3 days of CSF1 or saline i.t. injection.

2021-09-27 | GSE184799 | GEO

Translational control in the spinal cord regulates gene expression and pain hypersensitivity in the chronic phase of neuropathic pain

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

Single-cell RNA sequencing reveals cellular heterogeneity of spinal microglia in neuropathic pain

Project description:Recent studies reveal that microglia modulate synaptic transmission by direct synaptic pruning. Microglia reactivation is a crucial mechanism of central sensitization in neuropathic pain, yet the exact changes of microglia during the development of neuropathic pain and its interaction with the spinal inhibitory circuits remains unclear. In this work, single-cell sequencing delineates temporal changes in spinal microglia and identifies a specific type of microglia as the subpopulation mediating synaptic pruning. We found that peripheral nerve injury induced the transition of spinal microglia from a pro-inflammatory to a “pruning” state, resulting in pain hypersensitivity by spinal disinhibition.

2024-10-24 | GSE246288 | GEO

HDAC inhibitors attenuate the development of hypersensitivity in models of neuropathic pain [DRG tissue]

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. Injured ipsilateral DRG after L5 spinal nerve transection. Spinal cord tissue was run in a separate Affymetrix experiment.

2013-10-01 | E-GEOD-51295 | biostudies-arrayexpress

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