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The single-cell transcriptomic atlas iPain identifies senescence of nociceptors as a therapeutical target for chronic pain treatment

ABSTRACT: The single-cell transcriptomic atlas iPain identifies senescence of nociceptors as a therapeutical target for chronic pain treatment

PROVIDER: PRJNA1065374 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27563622_1.fastq.gz	Fastqsanger.gz
	SRR27563622_2.fastq.gz	Fastqsanger.gz
	SRR27563623_1.fastq.gz	Fastqsanger.gz
	SRR27563623_2.fastq.gz	Fastqsanger.gz
	SRR27563624_1.fastq.gz	Fastqsanger.gz

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The single-cell transcriptomic atlas iPain identifies senescence of nociceptors as a therapeutical target for chronic pain treatment

Project description:Chronic pain remains a significant medical challenge with complex underlying mechanisms, and an urgent need for new treatments. Our research built and utilized the iPain single-cell atlas to study chronic pain progression in dorsal root and trigeminal ganglia. We discovered that senescence of a small subset of pain-sensing neurons may be a key driver of chronic pain. This mechanism was observed in animal models after nerve injury and in human patients with chronic pain or diabetic neuropathy. Notably, treatment with senolytics, drugs that remove senescent cells, reversed pain symptoms in mice post-injury. These findings highlight the crucial role of cellular senescence in chronic pain development, demonstrate the therapeutic potential of senolytic treatments, and underscore the value of the iPain atlas for future pain research.

2024-07-19 | GSE253345 | GEO

Proteomics on Nav1.8-positive nociceptors of mouse DRG

Project description:Nociceptors play an essential role in both acute pain and chronic pain conditions. In this study, we examined the proteome of mouse dorsal root ganglia and compared NaV1.8Cre+/-; ROSA26-flox-stop-flox-DTA (Diphtheria toxin fragment A) mutant mice (NaV1.8Cre-DTA), in which NaV1.8-positive neurons (mainly nociceptors) in dorsal root ganglia (DRG) were ablated, with respective littermate wildtype controls.

2022-10-03 | PXD034447 | Pride

Identification by RNA-seq of Prdm12 regulated genes in dorsal root ganglia nociceptors of adult mice

Project description:Loss of Prdm12 increases formalin induced inflammatory pain by remodeling gene expression in mature nociceptors

2022-01-25 | GSE166062 | GEO

Nociceptor translational profiling reveals the RagA-mTORC1 network as a critical generator of neuropathic pain

Project description:Pain sensing neurons, nociceptors, are key drivers of neuropathic pain. We used translating ribosome affinity purification (trap) to comprehensively characterize up- and down-regulated mRNA translation in Scn10a-positive nociceptors in chemotherapy-induced neuropathic pain. We provide evidence that an underlying mechanism driving these changes in gene expression is a sustained mTORC1 activation driven by MNK1-eIF4E signaling. RagA, a GTPase controlling mTORC1 activity, is identified as a novel target of MNK1-eIF4E signaling, demonstrating a new link between these distinct signaling pathways. Neuropathic pain and RagA translation are strongly attenuated by genetic ablation of eIF4E phosphorylation, MNK1 elimination or treatment with the MNK inhibitor eFT508. We reveal a novel translational circuit for the genesis of neuropathic pain with important implications for next generation neuropathic pain therapeutics.

2018-08-01 | GSE113941 | GEO

mTOR-neuropeptide Y signaling sensitizes nociceptors to drive neuropathic pain development

Project description:Neuropathic pain is a refractory condition that involves de novo protein synthesis in the nociceptive pathway. The mechanistic target of rapamycin (mTOR) is a master regulator of protein synthesis; however, mechanisms underlying its role in neuropathic pain remain elusive. Using spared nerve injury-induced neuropathic pain model, we found mTOR activation in large-diameter dorsal root ganglion (DRG) neurons and spinal microglia. However, selective ablation of mTOR in DRG neurons, rather than microglia, alleviated neuropathic pain. Combining transcriptomic profiling, electrophysiological recording and pharmacologic manipulations, we demonstrated that activated mTOR promoted neuropeptide Y (NPY) induction in mechanoreceptors and that NPY acted on Y2 receptors (Y2R) but not Y1R to enhance nociceptor excitability. Peripheral replenishment of NPY reversed pain alleviation upon mTOR removal, whereas Y2R antagonists prevented its function. Our findings reveal an unexpected link between mTOR and NPY in promoting nociceptor sensitization and neuropathic pain, through NPY/Y2R signaling-mediated intra-ganglionic transmission.

2022-09-01 | GSE184014 | GEO

RRBS-based blood methylome in chronic nociceptive (NOCI) and neuropathic (NEURO) pain suffering patients and controls (CTL).

Project description:Nociceptive pain implies the activation of the nociceptors without damage to the somatosensory nervous system. Neuropathic pain implies an injury or a disease of the central or peripheral nervous system. Epigenomic may participate in chronic pain conditions as well as in the transition from acute to chronic pain. The purpose of the present study is to analyze how blood methylome differs in both mentionned types of chronic pain, by comparing them together and to controls. The study protocol was approved by the local ethic committee (CCVEM 034/12) and was conducted according to the recommendation of the Declaration of Helsinki. Patients were enrolled at the Clinique romande de réadaptation (CRR) in Sion, in Switzerland. Data were hosted and analyzed at the University of Geneva, Faculty of Medicine, Department of Genetic Medicine and Development, in Switzerland. Data were processed in the high performance computing cluster (HPC) nammed "Baobab" in the Geneva University.

2021-09-13 | GSE166255 | GEO

Peptides encoded by 5’ untranslated regions mediate pain sensitization

Project description:Nociceptors are neurons responsible for the detection of pain producing stimuli. Persistent changes in their activity, termed plasticity, benefit survival through injury avoidance and are regulated on a translational basis. Yet, the mRNAs whose translation facilitates plasticity are unknown. Here, we apply ribosome profiling to dorsal root ganglion and identify a small number of transcripts that are selectively translated in response to plasticity mediators. Among them are Arc and Fos, genes implicated in episodic learning in the brain. We demonstrate that the ribosomal S6 kinase 1 is responsible for their production in nociceptors. Blocking S6 driven translation also reduces pain associated behavioral responses in vivo. In addition to translation of coding regions of mRNA, we detect pervasive ribosome occupancy in 5’ untranslated regions. We find that peptides encoded by open reading frames in the 5’ untranslated regions of Calca and Egr2 increase neuronal excitability in vitro and are sufficient to induce pain-like behaviors in vivo. Together, our findings uncover new targets of translational control that drive changes in plasticity and suggest new mechanisms for targeted pain therapeutics that disrupt pain signaling.

2020-02-01 | GSE117043 | GEO

MicroRNA-183 cluster continuously scales mechanical pain sensitivity by regulating basal and neuropathic pain gene pathways.

Project description:Nociception is protective and prevents tissue damage but can also facilitate chronic pain. If a general principle governs these two types of pain is unknown. Here, we show that both basal mechanical and neuropathic pain are controlled by microRNA-183 cluster in mice. This single cluster controls more than 80% of neuropathic pain-regulated genes and scales basal mechanical sensitivity and mechanical allodynia by regulating auxiliary voltage-gated calcium channel subunits a2d. Basal sensitivity is controlled in nociceptors and allodynia involves TrkB+ light-touch mechanoreceptors. These light-touch sensitive neurons that normally do not elicit pain produce pain during neuropathy that is reversed by gabapentin. Thus, a single miRNA cluster continuously scales acute noxious mechanical sensitivity in nociceptive neurons and suppresses neuropathic pain transduction in a specific, light-touch sensitive neuronal type recruited during mechanical allodynia.

2017-05-25 | GSE99265 | GEO

Induction of antiviral Interferon-Stimulated Genes (ISGs) by neuronal STING promotes the resolution of pain

Project description:Nociceptive neurons respond to inflammation, initiating protective reflexes and alerting the host. Here we found that TRPV1 nociceptors express and activate the cytosolic DNA-sensing protein Stimulator of Interferon Genes (STING) in response to inflammation. Neuronal activation of STING promotes signaling through TBK1 and triggers a Type I interferon (IFN-I) response. The absence of STING led to heightened pain responses to chemical irritants or heat. In contrast, mice expressing a nociceptor-specific gain-of-function mutation in STING exhibited an IFN gene signature that reduced nociceptor excitability and inflammatory hyperalgesia. Importantly, several IFN-regulated genes (IRGs) were specific to nociceptor ion channels responsible for controlling neuronal activity and pain threshold. Therefore, STING promotes a pain-resolving IFN-I signaling pathway in nociceptors, thereby preventing sensitization and persistent pain

2023-08-05 | GSE236865 | GEO

Effect of nociceptors on dendritic cells

Project description:We explored the effects of nociceptors on DC under various conditions by means of in vitro coculture of Flt3L-induced bone marrow-derived DCs and primary mouse nociceptors.

2023-04-01 | GSE217500 | GEO

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