ArticlePurinergic signalling2016
LncRNA uc.48+ is involved in diabetic neuropathic pain mediated by the P2X3 receptor in the dorsal root ganglia.
Article in Purinergic signalling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.
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Who cites it
61 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- The etiological roles of miRNAs, lncRNAs, and circRNAs in neuropathic pain: A narrative review.Journal of clinical laboratory analysis · 2022Pooled it
- Epigenetic modifications associated to diabetic peripheral neuropathic pain (Review).Molecular medicine reports · 2025Review
- Metabolic memory: mechanisms and diseases.Signal transduction and targeted therapy · 2024Review
- Functional nucleic acids for the treatment of diabetic complications.Nanoscale advances · 2023Review
- Ultra-conserved RNA: a novel biological tool with diagnostic and therapeutic potential.Discover oncology · 2023Review
- Diabetic Polyneuropathy: New Strategies to Target Sensory Neurons in Dorsal Root Ganglia.International journal of molecular sciences · 2023Review
- Analgesic effect of electroacupuncture on bone cancer pain in rat model: the role of peripheral P2X3 receptor.Purinergic signalling · 2023Article
- Long non-coding RNA MSTRG.81401 short hairpin RNA relieves diabetic neuropathic pain and behaviors of depression by inhibiting P2X4 receptor expression in type 2 diabetic rats.Purinergic signalling · 2023Article
- Review
- Blockage of HCN Channels Inhibits the Function of P2X Receptors in Rat Dorsal Root Ganglion Neurons.Neurochemical research · 2022Article
- Ion channel long non-coding RNAs in neuropathic pain.Pflugers Archiv : European journal of physiology · 2022Review
- Exploring neuronal mechanisms involved in the scratching behavior of a mouse model of allergic contact dermatitis by transcriptomics.Cellular & molecular biology letters · 2022Article
- The emerging power and promise of non-coding RNAs in chronic pain.Frontiers in molecular neuroscience · 2022Review
- Long non-coding RNAs in metabolic disorders: pathogenetic relevance and potential biomarkers and therapeutic targets.Journal of endocrinological investigation · 2021Review
- Downregulation of a Dorsal Root Ganglion-Specifically Enriched Long Noncoding RNA is Required for Neuropathic Pain by Negatively Regulating RALY-Triggered Ehmt2 Expression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Microdeletion of 9q22.3: A patient with minimal deletion size associated with a severe phenotype.American journal of medical genetics. Part A · 2021Article
- Genetic and Epigenomic Modifiers of Diabetic Neuropathy.International journal of molecular sciences · 2021Review
- Transcriptome profiling of long noncoding RNAs and mRNAs in spinal cord of a rat model of paclitaxel-induced peripheral neuropathy identifies potential mechanisms mediating neuroinflammation and pain.Journal of neuroinflammation · 2021Article
- Downregulation of lncRNA FIRRE relieved the neuropathic pain of female mice by suppressing HMGB1 expression.Molecular and cellular biochemistry · 2021Article
- Roles of Long Non-coding RNAs in the Development of Chronic Pain.Frontiers in molecular neuroscience · 2021Review
1 more citing papers are in PubMed but not listed here.
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17 authors at 1 institution in 1 country.
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Abstract
Some long non-coding RNAs (lncRNAs) participate in physiological processes that maintain cellular and tissue homeostasis, and thus, the dysregulated expression of lncRNAs is involved in the onset and progression of many pathological conditions. Research has indicated that the genetic knockout of some lncRNAs in mice resulted in peri- or postnatal lethality or developmental defects. Diabetes mellitus (DM) is a major cause of peripheral neuropathy. Our studies showed that the expression levels of lncRNA uc.48+ in the diabetic rat dorsal root ganglia (DRG) and the DM patients' serum samples were increased. It suggested that lncRNA uc.48+ was involved in the pathophysiological process of DM. The aim of this study was to investigate the effects of lncRNA uc.48+ small interfering RNA (siRNA) on diabetic neuropathic pain (DNP) mediated by the P2X3 receptor in the DRG. The values of the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were measured by the von Frey test and Hargreaves' test, respectively. The levels of P2X3 protein and messenger RNA (mRNA) in the DRG were detected by reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemistry, and western blotting. The experiments showed that the MWT and TWL values in DM rats were lower than those in the control rats. The MWT and TWL values in DM rats treated with lncRNA uc.48+ siRNA were increased compared to those in DM rats, but there was no significant difference between the DM rat group and the DM + scramble siRNA group. The levels of P2X3 protein and mRNA in the DM DRG were higher than those in the control, while the levels of P2X3 protein and mRNA in the DG of DM rats treated with uc.48+ siRNA were significantly decreased compared to those in DM rats. The expression levels of TNF-α in the DRG of DM rats treated with uc.48+ siRNA were significantly decreased compared to those in the DM group. The phosphorylation and activation of ERK1/2 in the DM DRG were decreased by uc.48+ siRNA treatment. Therefore, uc.48+ siRNA treatment may alleviate the DNP by inhibiting the excitatory transmission mediated by the P2X3 receptor in DRG.
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