ArticleJournal of neuroinflammation2020
Hypomethylation of nerve growth factor (NGF) promotes binding of C/EBPα and contributes to inflammatory hyperalgesia in rats.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 53 citations in OpenAlex.
- Neuropsychiatric drug development in China: Current status and emerging trends.Molecular psychiatry · 2026Review
- NGF/ERK signaling-mediated epigenetic regulation of neuropathic pain in the cerebrospinal fluid-contacting nucleus.Frontiers in neurology · 2025Article
- Pain - related methylation driver genes affect the prognosis of pancreatic cancer patients by altering immune function and perineural infiltration.Frontiers in genetics · 2025Article
- Targeting nerve growth factor for pain relief: pros and cons.The Korean journal of pain · 2024Review
- DUSP5 regulated by YTHDF1-mediated m6A modification promotes epithelial-mesenchymal transition and EGFR-TKI resistance via the TGF-β/Smad signaling pathway in lung adenocarcinoma.Cancer cell international · 2024Article
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- The dorsal root ganglion as a target for neurorestoration in neuropathic pain.Neural regeneration research · 2024Review
- Nerve Growth Factor and the Role of Inflammation in Tumor Development.Current issues in molecular biology · 2024Review
- Identification and validation of aging-related genes in neuropathic pain using bioinformatics.Frontiers in genetics · 2024Article
- Pathophysiology of Pain and Mechanisms of Neuromodulation: A Narrative Review (A Neuron Project).Journal of pain research · 2024Review
- Changes in serum levels of pain mediators in hemiplegic shoulder pain.Brain and behavior · 2023Article
- Neuronal Differentiation and Outgrowth Effect of Thymol inInternational journal of molecular sciences · 2023Article
- A Review of Molecular Interplay between Neurotrophins and miRNAs in Neuropsychological Disorders.Molecular neurobiology · 2022Review
- Role of Epigenetic Mechanisms in Chronic Pain.Cells · 2022Review
- The neuronal tyrosine kinase receptor ligand ALKAL2 mediates persistent pain.The Journal of clinical investigation · 2022Article
- DNA Methylation and Non-Coding RNAs during Tissue-Injury Associated Pain.International journal of molecular sciences · 2022Review
- Article
- Integrated Analysis of Omics Data Reveal AP-1 as a Potential Regulation Hub in the Inflammation-Induced Hyperalgesia Rat Model.Frontiers in immunology · 2021Article
- CaMolecular pharmacologyArticle
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundChronic pain usually accompanied by tissue damage and inflammation. However, the pathogenesis of chronic pain remains unclear.
methodsWe investigated the role of nerve growth factor (NGF) in chronic inflammatory pain induced by complete Freund's adjuvant (CFA), explored the methylation status of CpG islands in the promoter region of the NGF gene, and clarified the function and mechanism of C/EBPα-NGF signaling pathway from epigenetic perspective in the chronic inflammatory pain model.
resultsCFA induced significant hyperalgesia and continuous upregulation of NGF mRNA and protein levels in the L4-6 dorsal root ganglions (DRGs) in rats. Hypomethylation of CpG islands occurred in the NGF gene promoter region after CFA treatment. At the same time, the miR-29b expression level was significantly increased, while the DNA methyltransferase 3b (DNMT3b) level reduced significantly. Moreover, CFA treatment promoted binding of C/EBPα to the NGF gene promoter region and C/EBPα siRNA treatment obviously decreased expression of NGF levels and also alleviate inflammatory hyperalgesia significantly in rats.
conclusionCollectively, the results indicated that CFA leads to the upregulation of miR-29b level, which represses the expression of DNMT3b, enhances the demethylation of the NGF gene promoter region, and promotes the binding of C/EBPα with the NGF gene promoter, thus results in the upregulation of NGF gene expression and maintenance of chronic inflammatory pain.
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