ArticleFrontiers in molecular neuroscience2017
MiR-30b Attenuates Neuropathic Pain by Regulating Voltage-Gated Sodium Channel Nav1.3 in Rats.
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- The etiological roles of miRNAs, lncRNAs, and circRNAs in neuropathic pain: A narrative review.Journal of clinical laboratory analysis · 2022Pooled it
- Ion channel and biophysical properties of extracellular vesicles.The Journal of biological chemistry · 2026Review
- A comprehensive review on pain: Model, target, therapy, and prospect (Review).International journal of molecular medicine · 2026Review
- Alteration of microRNA Expression Associated with Chronic Back Pain in Patients with Intervertebral Disc Degeneration: A Scoping Review.International journal of molecular sciences · 2026Article
- Article
- Modulation of ion channels as emerging therapeutic targets in the treatment of diabetic neuropathy.EXCLI journal · 2026Review
- MicroRNA-Based Delivery Systems for Chronic Neuropathic Pain Treatment in Dorsal Root Ganglion.Pharmaceutics · 2025Review
- Article
- Exosome-mediated miRNA delivery: a molecular switch for reshaping neuropathic pain therapy.Frontiers in molecular neuroscience · 2025Review
- Nanomedicine and voltage-gated sodium channel blockers in pain management: a game changer or a lost cause?Drug delivery and translational research · 2024Review
- Description of Novel Molecular Factors in Lumbar DRGs and Spinal Cord Factors Underlying Development of Neuropathic Pain Component in the Animal Model of Osteoarthritis.Molecular neurobiology · 2024Article
- Metabolic memory: mechanisms and diseases.Signal transduction and targeted therapy · 2024Review
- Cav3.2 T-Type calcium channels downregulation attenuates bone cancer pain induced by inhibiting IGF-1/HIF-1α signaling pathway in the rat spinal cord.Journal of bone oncology · 2023Article
- Integrative miRNA-mRNA profiling of human epidermis: unique signature of SCN9A painful neuropathy.Brain : a journal of neurology · 2023Article
- Research hotspots and trends on spinal cord stimulation for pain treatment: a two-decade bibliometric analysis.Frontiers in neuroscience · 2023Article
- Emerging roles of miRNAs in neuropathic pain: From new findings to novel mechanisms.Frontiers in molecular neuroscience · 2023Review
- Structure-function and rational design of a spider toxin Ssp1a at human voltage-gated sodium channel subtypes.Frontiers in pharmacology · 2023Article
- Neuropathic pain; what we know and what we should do about it.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- Upregulation of NaCells · 2022Article
- MiR-106b-5p Attenuates Neuropathic Pain by Regulating the P2X4 Receptor in the Spinal Cord in Mice.Journal of molecular neuroscience : MN · 2022Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Nav1.3 is a tetrodotoxin-sensitive isoform among voltage-gated sodium channels that are closely associated with neuropathic pain. It can be up-regulated following nerve injury, but its biological function remains uncertain. MicroRNAs (miRNAs) are endogenous non-coding RNAs that can regulate post-transcriptional gene expression by binding with their target mRNAs. Using Target Scan software, we discovered that SCN3A is the major target of miR-30b, and we then determined whether miR-30b regulated the expression of Nav1.3 by transfecting miR-30b agomir through the stimulation of TNF-α or by transfecting miR-30b antagomir in primary dorsal root ganglion (DRG) neurons. The spinal nerve ligation (SNL) model was used to determine the contribution of miR-30b to neuropathic pain, to evaluate changes in Nav1.3 mRNA and protein expression, and to understand the sensitivity of rats to mechanical and thermal stimuli. Our results showed that miR-30b agomir transfection down-regulated Nav1.3 mRNA stimulated with TNF-α in primary DRG neurons. Moreover, miR-30b overexpression significantly attenuated neuropathic pain induced by SNL, with decreases in the expression of Nav1.3 mRNA and protein both in DRG neurons and spinal cord. Activation of Nav1.3 caused by miR-30b antagomir was identified. These data suggest that miR-30b is involved in the development of neuropathic pain, probably by regulating the expression of Nav1.3, and might be a novel therapeutic target for neuropathic pain.
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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.