ArticleMolecular pain2016
MicroRNA-30b regulates expression of the sodium channel Nav1.7 in nerve injury-induced neuropathic pain in the rat.
Article in Molecular pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 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
- Decoding orofacial pain: a translational review of mechanisms and novel therapies.The journal of headache and pain · 2025Review
- MicroRNA-Based Delivery Systems for Chronic Neuropathic Pain Treatment in Dorsal Root Ganglion.Pharmaceutics · 2025Review
- Burn scar pain: from mechanisms to treatments.Frontiers in physiology · 2025Review
- Selective neural inhibition via photobiomodulation alleviates behavioral hypersensitivity associated with small sensory fiber activation.Lasers in surgery and medicine · 2024Article
- Communicating pain: emerging axonal signaling in peripheral neuropathic pain.Frontiers in neuroanatomy · 2024Review
- Narrative Review of the Complex Interaction between Pain and Trauma in Children: A Focus on Biological Memory, Preclinical Data, and Epigenetic Processes.Children (Basel, Switzerland) · 2023Review
- Integrative miRNA-mRNA profiling of human epidermis: unique signature of SCN9A painful neuropathy.Brain : a journal of neurology · 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
- The Yin/Yang Balance of Communication between Sensory Neurons and Macrophages in Traumatic Peripheral Neuropathic Pain.International journal of molecular sciences · 2022Review
- Role of Epigenetic Mechanisms in Chronic Pain.Cells · 2022Review
- Role of miRNAs in diabetic neuropathy: mechanisms and possible interventions.Molecular neurobiology · 2022Review
- The emerging power and promise of non-coding RNAs in chronic pain.Frontiers in molecular neuroscience · 2022Review
- The different mechanisms of peripheral and central TLR4 on chronic postsurgical pain in rats.Journal of anatomy · 2021Article
- Long-lasting analgesia via targeted in situ repression of NaScience translational medicine · 2021Article
- Article
- New Vistas in microRNA Regulatory Interactome in Neuropathic Pain.Frontiers in pharmacology · 2021Review
- microRNA-Based Network and Pathway Analysis for Neuropathic Pain in Rodent Models.Frontiers in molecular biosciences · 2021Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated sodium channels, which are involved in pain pathways, have emerged as major targets for therapeutic intervention in pain disorders. Nav1.7, the tetrodotoxin-sensitive voltage-gated sodium channel isoform encoded by SCN9A and predominantly expressed in pain-sensing neurons in the dorsal root ganglion, plays a crucial role in nociception. MicroRNAs are highly conserved, small non-coding RNAs. Through binding to the 3' untranslated region of their target mRNAs, microRNAs induce the cleavage and/or inhibition of protein translation. Based on bioinformatics analysis using TargetScan software, we determined that miR-30b directly targets SCN9A To investigate the roles of Nav1.7 and miR-30b in neuropathic pain, we examined changes in the expression of Nav1.7 in the dorsal root ganglion by miR-30b over-expression or knockdown in rats with spared nerve injury. Our results demonstrated that the expression of miR-30b and Nav1.7 was down-regulated and up-regulated, respectively, in the dorsal root ganglion of spared nerve injury rats. MiR-30b over-expression in spared nerve injury rats inhibited SCN9A transcription, resulting in pain relief. In addition, miR-30b knockdown significantly increased hypersensitivity to pain in naive rats. We also observed that miR-30b decreased Nav1.7 expression in PC12 cells. Taken together, our results suggest that miR-30b plays an important role in neuropathic pain by regulating Nav1.7 expression. Therefore, miR-30b may be a promising target for the treatment of chronic neuropathic pain.
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