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

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

PROVIDER: PRJNA766540 | ENA |

REPOSITORIES: ENA

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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

| PRJNA766536 | ENA

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

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

| PRJNA766541 | ENA

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

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

Project description: Not available

| S-EPMC8639143 | biostudies-literature

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

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-09-27 | GSE184801 | 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

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

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

HDAC inhibitors attenuate the development of hypersensitivity in models of neuropathic pain [spinal cord 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. 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

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