ArticleThe Journal of experimental medicine2021
ZNF382 controls mouse neuropathic pain via silencer-based epigenetic inhibition of Cxcl13 in DRG neurons.
Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- The impactful role of the HDACs in the regulation of gene expression and as targets for disease therapy.Science advances · 2026Review
- Spinal Cord CELF4 in Chronic Constriction Injury-Induced Neuropathic Pain: Association with TRPV1 and COX-2 Expression.Journal of molecular neuroscience : MN · 2026Article
- Single-cell polygenic risk scores dissect cellular and molecular heterogeneity of complex human diseases.Nature biotechnology · 2026Article
- Hyodeoxycholic acid relieves neuropathic pain by activating farnesoid X receptor signaling.Journal of advanced research · 2026Article
- A GABAergic Projection from the Zona Incerta to the Rostral Ventromedial Medulla Modulates Descending Control of Neuropathic Pain.Brain sciences · 2026Article
- Bioinformatics-based identification of potential genes in the thalamus associated with chronic orofacial and somatic inflammatory pain.Frontiers in neuroscience · 2026Article
- ZFP612 controls neuropathic pain through epigenetic repression of Il1rl1 within the silencer-promoter loop in primary sensory neurons of male mice.Nature communications · 2025Article
- CXCL13/CXCR5: a new target for pain treatment.International journal of surgery (London, England) · 2025Review
- SERBP1-PCIF1 complex-controlled m6Am modification in glutamatergic neurons of the primary somatosensory cortex is required for neuropathic pain in mice.Nature communications · 2025Article
- The dual roles of chemokines in peripheral nerve injury and repair.Inflammation and regeneration · 2025Review
- An atlas of neuropathic pain-associated molecular pathological characteristics in the mouse spinal cord.Communications biology · 2025Article
- Rational design of indoleamine 2,3-dioxygenase 1 (IDO1) inhibitors featuring 1,2,3-triazole derivatives with enhanced anti-inflammatory and analgesic efficacy.Frontiers in pharmacology · 2025Article
- Histone modifications and Sp1 promote GPR160 expression in bone cancer pain within rodent models.EMBO reports · 2024Article
- Chemokine CXCL13-CXCR5 signaling in neuroinflammation and pathogenesis of chronic pain and neurological diseases.Cellular & molecular biology letters · 2024Review
- CXCL13: a common target for immune-mediated inflammatory diseases.Clinical and experimental medicine · 2024Review
- Interleukin-22 receptor 1-mediated stimulation of T-type CaCell communication and signaling : CCS · 2024Article
- The Epigenetics of Neuropathic Pain: A Systematic Update.International journal of molecular sciences · 2023Review
- Targeting sensory neuron GPCRs for peripheral neuropathic pain.Trends in pharmacological sciences · 2023Review
- A sensory neuron-specific long non-coding RNA reduces neuropathic pain by rescuing KCNN1 expression.Brain : a journal of neurology · 2023Article
- Quantifying the arms race between LINE-1 and KRAB-zinc finger genes through TECookbook.NAR genomics and bioinformatics · 2023Article
Corrections and comments
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Authors and funding
20 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nerve injury-induced changes of gene expression in dorsal root ganglion (DRG) are critical for neuropathic pain genesis. However, how these changes occur remains elusive. Here we report the down-regulation of zinc finger protein 382 (ZNF382) in injured DRG neurons after nerve injury. Rescuing this down-regulation attenuates nociceptive hypersensitivity. Conversely, mimicking this down-regulation produces neuropathic pain symptoms, which are alleviated by C-X-C motif chemokine 13 (CXCL13) knockdown or its receptor CXCR5 knockout. Mechanistically, an identified cis-acting silencer at distal upstream of the Cxcl13 promoter suppresses Cxcl13 transcription via binding to ZNF382. Blocking this binding or genetically deleting this silencer abolishes the ZNF382 suppression on Cxcl13 transcription and impairs ZNF382-induced antinociception. Moreover, ZNF382 down-regulation disrupts the repressive epigenetic complex containing histone deacetylase 1 and SET domain bifurcated 1 at the silencer-promoter loop, resulting in Cxcl13 transcriptional activation. Thus, ZNF382 down-regulation is required for neuropathic pain likely through silencer-based epigenetic disinhibition of CXCL13, a key neuropathic pain player, in DRG neurons.
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