ArticleScientific reports2016
Tet1-dependent epigenetic modification of BDNF expression in dorsal horn neurons mediates neuropathic pain in rats.
Article in Scientific reports, 2016. 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, 77 citations in OpenAlex.
- Exercise, Demethylase FTO, Neurological Disorders, and Neuropathic Pain: Potential Molecular Mechanisms.CNS neuroscience & therapeutics · 2026Review
- TET1 downregulation in the dorsal root ganglion and spinal cord is required for short-term sleep disturbance to delay surgical pain recovery.British journal of anaesthesia · 2026Article
- Review
- Epigenetic, chromatin-associated, and epitranscriptomic regulation in chronic pain: mechanisms and translational prospects.Frontiers in genetics · 2026Review
- Exploring the epigenetic modifications of the RONS-TRPA1-CGRP axis in migraine pathophysiology.The journal of headache and pain · 2025Review
- Epigenetic Landscapes of Pain: DNA Methylation Dynamics in Chronic Pain.International journal of molecular sciences · 2024Review
- The Epigenetics of Neuropathic Pain: A Systematic Update.International journal of molecular sciences · 2023Review
- Intraperitoneal 5-Azacytidine Alleviates Nerve Injury-Induced Pain in Rats by Modulating DNA Methylation.Molecular neurobiology · 2023Article
- Association between single nucleotide variants and severe chronic pain in older adult patients after lower extremity arthroplasty.Journal of orthopaedic surgery and research · 2023Article
- RNA interference-mediated silencing of DNA methyltransferase 1 attenuates neuropathic pain by accelerating microglia M2 polarization.BMC neurology · 2022Article
- TET1-induced DNA demethylation in dentate gyrus is important for reward conditioning and reinforcement.Molecular neurobiology · 2022Article
- DNA Methylation and Non-Coding RNAs during Tissue-Injury Associated Pain.International journal of molecular sciences · 2022Review
- DNA Methylation: A Target in Neuropathic Pain.Frontiers in medicine · 2022Review
- The Epigenetic Mechanisms Involved in Chronic Pain in Rodents: A Mini- Review.Current neuropharmacology · 2022Review
- Non-coding RNA and n6-methyladenosine modification play crucial roles in neuropathic pain.Frontiers in molecular neuroscience · 2022Review
- Article
- Blocking the Spinal Fbxo3/CARM1/KNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Role of Melatonin in the Regulation of Pain.Journal of pain research · 2020Review
- TET1 Overexpression Mitigates Neuropathic Pain Through Rescuing the Expression of μ-Opioid Receptor and Kv1.2 in the Primary Sensory Neurons.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Article
- Perinatal Bisphenol A Exposure and Reprogramming of Imprinted Gene Expression in the Adult Mouse Brain.Frontiers in genetics · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ten-eleven translocation methylcytosine dioxygenase 1 (Tet1) mediates the conversion of 5-methylcytosine (5 mC) to 5-hydroxymethylcytosine (5 hmC), hence promoting DNA demethylation. Although recent studies have linked the DNA demethylation of specific genes to pain hypersensitivity, the role of spinal Tet1-dependent DNA demethylation in nociception hypersensitivity development remains elusive. Here, we report correlated with behavioral allodynia, spinal nerve ligation (SNL) upregulated Tet1 expression in dorsal horn neurons that hydroxylate 5 mC to 5 hmC at CpG dinucleotides in the bdnf promoter to promote spinal BDNF expression at day 7 after operation. Focal knockdown of spinal Tet1 expression decreased Tet1 binding and 5 hmC enrichment, further increased 5 mC enrichment at CpG sites in the bdnf promoter and decreased spinal BDNF expression accompanied by the alleviation of the developed allodynia. Moreover, at day 7 after operation, SNL-enhanced Tet1 expression also inhibited the binding of DNA methyltransferases (DNMTs, i.e., DNMT1, DNMT3a, and DNMT3b) to the bdnf promoter, a requirement for transcriptional silencing by catalysing 5-cytosine (5C) to 5 mC. Together, these data suggest at CpG sites of the bdnf promoter, SNL-enhanced Tet1 expression promotes DNA demethylation both by converting 5 mC to 5 hmC and inhibiting DNMT binding to regulate spinal BDNF expression, hence contributing to behavioral allodynia development.
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