ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Epigenetic modification of spinal miR-219 expression regulates chronic inflammation pain by targeting CaMKIIγ.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 104 citations in OpenAlex.
- Regulation of miR-219 and its target RalGPS dictates acute synaptic plasticity at thebioRxiv : the preprint server for biology · 2025Article
- Role of ncRNAs in the Development of Chronic Pain.Non-coding RNA · 2025Review
- The Receptor for Advanced Glycation End-products in the Mouse Anterior Cingulate Cortex is Involved in Neuron‒Astrocyte Coupling in Chronic Inflammatory Pain and Anxiety Comorbidity.Molecular neurobiology · 2025Article
- H3K27 Trimethylation-Mediated Downregulation of miR-216a-3p in Sensory Neurons Regulates Neuropathic Pain Behaviors via Targeting STIM1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Predictive and concurrent validity of pain sensitivity phenotype, neuropeptidomics and neuroepigenetics in the MI-RAT osteoarthritic surgical model in rats.Frontiers in cell and developmental biology · 2024Article
- Upregulation of lysine-specific demethylase 6B aggravates inflammatory pain through H3K27me3 demethylation-dependent production of TNF-α in the dorsal root ganglia and spinal dorsal horn in rats.CNS neuroscience & therapeutics · 2023Article
- Downregulation of ciRNA-Kat6b in dorsal spinal horn is required for neuropathic pain by regulating Kcnk1 in miRNA-26a-dependent manner.CNS neuroscience & therapeutics · 2023Article
- Differential functions of RhoGDIβ in malignant transformation and progression of urothelial cell following N-butyl-N-(4-hydmoxybutyl) nitrosamine exposure.BMC biology · 2023Article
- Altered Brain Expression of DNA Methylation and Hydroxymethylation Epigenetic Enzymes in a Rat Model of Neuropathic Pain.International journal of molecular sciences · 2023Article
- Exosomes from Inflamed Macrophages Promote the Progression of Parkinson's Disease by Inducing Neuroinflammation.Molecular neurobiology · 2023Article
- The Role of miRNAs in Neuropathic Pain.Biomedicines · 2023Review
- Emerging roles of miRNAs in neuropathic pain: From new findings to novel mechanisms.Frontiers in molecular neuroscience · 2023Review
- Noncoding RNAs: Novel Targets for Opioid Tolerance.Current neuropharmacology · 2023Review
- The potential value of exosomes as adjuvants for novel biologic local anesthetics.Frontiers in pharmacology · 2023Review
- Activation of Dopamine D2 Receptors Alleviates Neuronal Hyperexcitability in the Lateral Entorhinal Cortex via Inhibition of HCN Current in a Rat Model of Chronic Inflammatory Pain.Neuroscience bulletin · 2022Article
- CaMKII Splice Variants in Vascular Smooth Muscle Cells: The Next Step or Redundancy?International journal of molecular sciences · 2022Review
- SIRT1: A promising therapeutic target for chronic pain.CNS neuroscience & therapeutics · 2022Review
- Extracellular vesicles derived from inflammatory-educated stem cells reverse brain inflammation-implication of miRNAs.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- DNA Methylation and Non-Coding RNAs during Tissue-Injury Associated Pain.International journal of molecular sciences · 2022Review
- miRNA-22 UpregulatesOxidative medicine and cellular longevity · 2022Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence has shown that miRNA-mediated gene expression modulation contributes to chronic pain, but its functional regulatory mechanism remains unknown. Here, we found that complete Freund's adjuvant (CFA)-induced chronic inflammation pain significantly reduced miRNA-219 (miR-219) expression in mice spinal neurons. Furthermore, the expression of spinal CaMKIIγ, an experimentally validated target of miR-219, was increased in CFA mice. Overexpression of spinal miR-219 prevented and reversed thermal hyperalgesia and mechanical allodynia and spinal neuronal sensitization induced by CFA. Concurrently, increased expression of spinal CaMKIIγ was reversed by miR-219 overexpression. Downregulation of spinal miR-219 in naive mice induced pain-responsive behaviors and increased p-NMDAR1 expression, which could be inhibited by knockdown of CaMKIIγ. Bisulfite sequencing showed that CFA induced the hypermethylation of CpG islands in the miR-219 promoter. Treatment with demethylation agent 5'-aza-2'-deoxycytidine markedly attenuated pain behavior and spinal neuronal sensitization, which was accompanied with the increase of spinal miR-219 and decrease of CaMKIIγ expression. Together, we conclude that methylation-mediated epigenetic modification of spinal miR-219 expression regulates chronic inflammatory pain by targeting CaMKIIγ.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.