ArticleMolecular pain2012
Reduction of voltage gated sodium channel protein in DRG by vector mediated miRNA reduces pain in rats with painful diabetic neuropathy.
Article in Molecular pain, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Identification and validation of MicroRNA-mRNA Networks in Dorsal Root Ganglia after Peripheral Nerve Injury.International journal of medical sciences · 2022Pooled it
- Chasing the Wrong Door for 30 Years: Is Suzetrigine the Key to Selective Pain Relief?Medicina (Kaunas, Lithuania) · 2026Review
- Epimutation analysis reveals involvement of SLIT2/ROBO signaling pathway in painful diabetic neuropathy.Human genomics · 2026Article
- MicroRNA-Based Delivery Systems for Chronic Neuropathic Pain Treatment in Dorsal Root Ganglion.Pharmaceutics · 2025Review
- Non-replicative herpes simplex virus genomic and amplicon vectors for gene therapy - an update.Gene therapy · 2025Review
- Epigenetic modifications associated to diabetic peripheral neuropathic pain (Review).Molecular medicine reports · 2025Review
- Voltage-gated sodium channels in diabetic sensory neuropathy: Function, modulation, and therapeutic potential.Frontiers in cellular neuroscience · 2022Review
- Keratinocyte Biomarkers Distinguish Painful Diabetic Peripheral Neuropathy Patients and Correlate With Topical Lidocaine Responsiveness.Frontiers in pain research (Lausanne, Switzerland) · 2021Article
- Manipulation of a spider peptide toxin alters its affinity for lipid bilayers and potency and selectivity for voltage-gated sodium channel subtype 1.7.The Journal of biological chemistry · 2020Article
- miR-300 mitigates cancer-induced bone pain through targeting HMGB1 in rat models.Genes & genomics · 2020Article
- Article
- Mining the NaBiochemical pharmacology · 2019Review
- Spinal miRNA-124 regulates synaptopodin and nociception in an animal model of bone cancer pain.Scientific reports · 2017Article
- miR‑199a‑3p is involved in the pathogenesis and progression of diabetic neuropathy through downregulation of SerpinE2.Molecular medicine reports · 2017Article
- Drugging the pain epigenome.Nature reviews. Neurology · 2017Review
- Synergistic regulation of serotonin and opioid signaling contributes to pain insensitivity in Nav1.7 knockout mice.Science signaling · 2017Article
- Current and Future Issues in the Development of Spinal Agents for the Management of Pain.Current neuropharmacology · 2017Review
- Roles of Voltage-Gated Tetrodotoxin-Sensitive Sodium Channels NaV1.3 and NaV1.7 in Diabetes and Painful Diabetic Neuropathy.International journal of molecular sciences · 2016Review
- Serum MicroRNA Signatures in Migraineurs During Attacks and in Pain-Free Periods.Molecular neurobiology · 2016Article
- MicroRNA-30b regulates expression of the sodium channel Nav1.7 in nerve injury-induced neuropathic pain in the rat.Molecular pain · 2016Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundPainful neuropathy is a common complication of diabetes. Previous studies have identified significant increases in the amount of voltage gated sodium channel isoforms Na(V)1.7 and Na(V)1.3 protein in the dorsal root ganglia (DRG) of rats with streptozotocin (STZ)-induced diabetes. We found that gene transfer-mediated release of the inhibitory neurotransmitters enkephalin or gamma amino butyric acid (GABA) from DRG neurons in diabetic animals reduced pain-related behaviors coincident with a reduction in Na(V)1.7 protein levels in DRG in vivo. To further evaluate the role of Na(V)α subunit levels in DRG in the pathogenesis of pain in diabetic neuropathy, we constructed a non-replicating herpes simplex virus (HSV)-based vector expressing a microRNA (miRNA) against Na(V)α subunits.
resultsSubcutaneous inoculation of the miRNA-expressing HSV vector into the feet of diabetic rats to transduce DRG resulted in a reduction in Na(V)α subunit levels in DRG neurons, coincident with a reduction in cold allodynia, thermal hyperalgesia and mechanical hyperalgesia.
conclusionsThese data support the role of increased Na(V)α protein in DRG in the pathogenesis of pain in diabetic neuropathy, and provide a proof-of-principle demonstration for the development of a novel therapy that could be used to treat intractable pain in patients with diabetic neuropathy.
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