ArticleMolecular medicine (Cambridge, Mass.)2020
LncRNA KCNA2-AS regulates spinal astrocyte activation through STAT3 to affect postherpetic neuralgia.
Article in Molecular medicine (Cambridge, Mass.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- The etiological roles of miRNAs, lncRNAs, and circRNAs in neuropathic pain: A narrative review.Journal of clinical laboratory analysis · 2022Pooled it
- Immunoinflammatory mechanisms and emerging therapies for postherpetic neuralgia.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Review
- Functional connectome gradient alterations in herpes zoster and postherpetic neuralgia: associations with gene expression profiles.The journal of headache and pain · 2026Article
- Development and External Validation of a Nomogram for Predicting Postherpetic Neuralgia Risk in Patients with Herpes Zoster: A Retrospective Cohort Study.Journal of pain research · 2026Article
- Post-Herpetic Neuralgia: Review of Pathophysiology, Mechanisms, and Drug Treatment.Current neuropharmacology · 2026Review
- Fire Acupuncture Combined with Pulse Radiofrequency Relieves Tactile Allodynia in Rats with Postherpetic Neuralgia.International journal of general medicine · 2025Article
- Roles of KCNA2 in Neurological Diseases: from Physiology to Pathology.Molecular neurobiology · 2024Review
- The role of non-coding RNAs in neuropathic pain.Pflugers Archiv : European journal of physiology · 2024Review
- Development of a Prediction Model and Corresponding Scoring Table for Postherpetic Neuralgia Using Six Machine Learning Algorithms: A Retrospective Study.Pain and therapy · 2024Article
- Exploring viral neuropathic pain: Molecular mechanisms and therapeutic implications.PLoS pathogens · 2024Review
- Excitatory and inhibitory neuronal signaling in inflammatory and diabetic neuropathic pain.Molecular medicine (Cambridge, Mass.) · 2023Review
- Preparation of Primary Mixed Glial Cell Cultures from Adult Mouse Spinal Cord Tissue.Current protocols · 2023Article
- Identification of key potassium channel genes of temporal lobe epilepsy by bioinformatics analyses and experimental verification.Frontiers in neurology · 2023Article
- Rodent models of postherpetic neuralgia: How far have we reached?Frontiers in immunology · 2023Review
- Ion channel long non-coding RNAs in neuropathic pain.Pflugers Archiv : European journal of physiology · 2022Review
- Article
- Roles of Long Non-coding RNAs in the Development of Chronic Pain.Frontiers in molecular neuroscience · 2021Review
- Differential Expression of Long Non-Coding RNAs and Their Role in Rodent Neuropathic Pain Models.Journal of pain research · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesPostherpetic neuralgia (PHN) is the most common complication of herpes zoster, but the mechanism of PHN is still unclear. Activation of spinal astrocytes is involved in PHN. Our study aims to explore whether lncRNA KCNA2 antisense RNA (KCNA2-AS) regulates spinal astrocytes in PHN through signal transducers and activators of transcription 3 (STAT3).
methodsVaricella zoster virus (VZV)-infected CV-1 cells were injected into rats to construct a PHN model. Primary spinal cord astrocytes were activated using S-Nitrosoglutathione (GSNO). Glial fibrillary acidic protein (GFAP; marker of astrocyte activation), phosphorylated STAT3 (pSTAT3), and KCNA2-AS were analyzed by immunofluorescence and RNA fluorescence in situ hybridization. RNA pull-down and RNA immunoprecipitation were used to detect binding of KCNA2-AS to pSTAT3.
resultsKCNA2-AS was highly expressed in the spinal cord tissue of PHN model rats, and was positively correlated with GFAP expression. GFAP was significantly increased in GSNO-induced cells, but the knockdown of KCNA2-AS reversed this result. Meanwhile, pSTAT3 was significantly increased in GSNO-induced cells, but knockdown of KCNA2-AS reduced pSTAT3 within the nucleus while the total pSTAT3 did not change significantly. pSTAT3 bound to KCNA2-AS and this binding increased with GSNO treatment. Furthermore, knockdown of KCNA2-AS in PHN model rats relieved mechanical allodynia.
conclusionDown-regulation of KCNA2-AS alleviates PHN partly by reducing the translocation of pSTAT3 cytoplasm to the nucleus and then inhibiting the activation of spinal astrocytes.
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