Regulatory T-cells inhibit microglia-induced pain hypersensitivity in female mice
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ABSTRACT:
PROVIDER: PRJNA766536 | ENA |
REPOSITORIES: ENA
Dataset's files
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| SRR16081355.fastq.gz | Fastqsanger.gz | |||
| SRR16081356.fastq.gz | Fastqsanger.gz | |||
| SRR16081358.fastq.gz | Fastqsanger.gz | |||
| SRR16081359.fastq.gz | Fastqsanger.gz | |||
| SRR16081360.fastq.gz | Fastqsanger.gz |
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Project description:Regulatory T-cells inhibit microglia-induced pain hypersensitivity in female mice [exp2]
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Project description:Regulatory T-cells inhibit microglia-induced pain hypersensitivity in female mice [exp1]
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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.
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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.
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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.
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Project description:This study aimed to investigate the regulatory mechanism of M2 microglial exosomes (M2-exosomes) on neuronal ferroptosis during the progression of neuropathic pain (NP). IL-4 was used to induce M2 polarization of resting BV2 microglia. Subsequently, M2-exosomes were extracted from M2-polarized microglia and then sequenced. We further performed high-throughput sequencing for BV2 microglia and N2a neuronal cells that were cocultured with M2-exosomes. The effects of M2-exosomes on microglia and neuronal cells were detected by qRT-PCR, western blot, immunofluorescence, and flow cytometry in vitro. For the in vivo experiments, NP model mice were constructed using the chronic constriction sciatic nerve injury (CCI) method and injected intrathecally with M2-exosomes. Pain behavior and neuronal ferroptosis in the NP model mice were then assessed. The in vitro experiments indicated that M2-exosomes inhibited BV2 microglial inflammation response. The sequencing results for N2a neuronal cells treated with M2-exosomes showed that ferroptosis and the MAPK signaling pathway were significantly enriched. We further demonstrated that M2-exosomes reversed erastin-induced neuronal ferroptosis and inhibited activation of the p38 MAPK pathway in neuronal cells. Specifically, M2-exosomes increased expression of the ferroptosis antagonist factor GPX4 and decreased lipid peroxidation and mitochondrial ferrous levels in neuronal cells. The in vivo experiments using the CCI model showed that M2-exosomes increased GPX4 expression in spinal cord neuronal cells, inhibited the increase in ferrous content, and alleviated hyperalgesia. Our findings suggest that M2-exosomes activate the GPX4 antioxidant factor and inhibit p38 MAPK signaling pathways in neuronal ferroptosis, thereby improving pain hypersensitivity in NP.
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Project description:This study aimed to investigate the regulatory mechanism of M2 microglial exosomes (M2-exosomes) on neuronal ferroptosis during the progression of neuropathic pain (NP). IL-4 was used to induce M2 polarization of resting BV2 microglia. Subsequently, M2-exosomes were extracted from M2-polarized microglia and then sequenced. We further performed high-throughput sequencing for BV2 microglia and N2a neuronal cells that were cocultured with M2-exosomes. The effects of M2-exosomes on microglia and neuronal cells were detected by qRT-PCR, western blot, immunofluorescence, and flow cytometry in vitro. For the in vivo experiments, NP model mice were constructed using the chronic constriction sciatic nerve injury (CCI) method and injected intrathecally with M2-exosomes. Pain behavior and neuronal ferroptosis in the NP model mice were then assessed. The in vitro experiments indicated that M2-exosomes inhibited BV2 microglial inflammation response. The sequencing results for N2a neuronal cells treated with M2-exosomes showed that ferroptosis and the MAPK signaling pathway were significantly enriched. We further demonstrated that M2-exosomes reversed erastin-induced neuronal ferroptosis and inhibited activation of the p38 MAPK pathway in neuronal cells. Specifically, M2-exosomes increased expression of the ferroptosis antagonist factor GPX4 and decreased lipid peroxidation and mitochondrial ferrous levels in neuronal cells. The in vivo experiments using the CCI model showed that M2-exosomes increased GPX4 expression in spinal cord neuronal cells, inhibited the increase in ferrous content, and alleviated hyperalgesia. Our findings suggest that M2-exosomes activate the GPX4 antioxidant factor and inhibit p38 MAPK signaling pathways in neuronal ferroptosis, thereby improving pain hypersensitivity in NP.
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Project description:This study aimed to investigate the regulatory mechanism of M2 microglial exosomes (M2-exosomes) on neuronal ferroptosis during the progression of neuropathic pain (NP). IL-4 was used to induce M2 polarization of resting BV2 microglia. Subsequently, M2-exosomes were extracted from M2-polarized microglia and then sequenced. We further performed high-throughput sequencing for BV2 microglia and N2a neuronal cells that were cocultured with M2-exosomes. The effects of M2-exosomes on microglia and neuronal cells were detected by qRT-PCR, western blot, immunofluorescence, and flow cytometry in vitro. For the in vivo experiments, NP model mice were constructed using the chronic constriction sciatic nerve injury (CCI) method and injected intrathecally with M2-exosomes. Pain behavior and neuronal ferroptosis in the NP model mice were then assessed. The in vitro experiments indicated that M2-exosomes inhibited BV2 microglial inflammation response. The sequencing results for N2a neuronal cells treated with M2-exosomes showed that ferroptosis and the MAPK signaling pathway were significantly enriched. We further demonstrated that M2-exosomes reversed erastin-induced neuronal ferroptosis and inhibited activation of the p38 MAPK pathway in neuronal cells. Specifically, M2-exosomes increased expression of the ferroptosis antagonist factor GPX4 and decreased lipid peroxidation and mitochondrial ferrous levels in neuronal cells. The in vivo experiments using the CCI model showed that M2-exosomes increased GPX4 expression in spinal cord neuronal cells, inhibited the increase in ferrous content, and alleviated hyperalgesia. Our findings suggest that M2-exosomes activate the GPX4 antioxidant factor and inhibit p38 MAPK signaling pathways in neuronal ferroptosis, thereby improving pain hypersensitivity in NP.
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Project description:This study aimed to investigate the regulatory mechanism of M2 microglial exosomes (M2-exosomes) on neuronal ferroptosis during the progression of neuropathic pain (NP). IL-4 was used to induce M2 polarization of resting BV2 microglia. Subsequently, M2-exosomes were extracted from M2-polarized microglia and then sequenced. We further performed high-throughput sequencing for BV2 microglia and N2a neuronal cells that were cocultured with M2-exosomes. The effects of M2-exosomes on microglia and neuronal cells were detected by qRT-PCR, western blot, immunofluorescence, and flow cytometry in vitro. For the in vivo experiments, NP model mice were constructed using the chronic constriction sciatic nerve injury (CCI) method and injected intrathecally with M2-exosomes. Pain behavior and neuronal ferroptosis in the NP model mice were then assessed. The in vitro experiments indicated that M2-exosomes inhibited BV2 microglial inflammation response. The sequencing results for N2a neuronal cells treated with M2-exosomes showed that ferroptosis and the MAPK signaling pathway were significantly enriched. We further demonstrated that M2-exosomes reversed erastin-induced neuronal ferroptosis and inhibited activation of the p38 MAPK pathway in neuronal cells. Specifically, M2-exosomes increased expression of the ferroptosis antagonist factor GPX4 and decreased lipid peroxidation and mitochondrial ferrous levels in neuronal cells. The in vivo experiments using the CCI model showed that M2-exosomes increased GPX4 expression in spinal cord neuronal cells, inhibited the increase in ferrous content, and alleviated hyperalgesia. Our findings suggest that M2-exosomes activate the GPX4 antioxidant factor and inhibit p38 MAPK signaling pathways in neuronal ferroptosis, thereby improving pain hypersensitivity in NP.
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