ArticleBioscience reports2020
Inhibition of lncRNA DILC attenuates neuropathic pain via the SOCS3/JAK2/STAT3 pathway.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Trans-spinal magnetic stimulation upregulates microglial SOCS3 to attenuate neuroinflammation in chronic constriction injury-induced neuropathic pain.Neural regeneration research · 2026Article
- Microglia-derived neuroinflammatory pathways in neuropathic pain.The Korean journal of pain · 2026Review
- Roles of noncoding RNAs in neuropathic pain.Pain reports · 2025Review
- Enhancer profiling uncovers Jmjd1c as an essential suppressor in neuropathic pain by targeting Socs3.Genes & diseases · 2025Article
- Role of ncRNAs in the Development of Chronic Pain.Non-coding RNA · 2025Review
- The Integrated Transcriptome Bioinformatics Analysis of Energy Metabolism-Related Profiles for Dorsal Root Ganglion of Neuropathic Pain.Molecular neurobiology · 2025Article
- Inhibition of histone deacetylase 6 alleviates neuropathic pain via direct regulating post-translation of spinal STAT3 and decreasing downstream C-C Motif Chemokine Ligand 7 synthesis.Journal of neuroinflammation · 2025Article
- LncRNA-Associated ceRNA Network in the Spinal Cord Reveals the Central Mechanism of Chronic Inflammatory Visceral Pain.Journal of pain research · 2025Article
- Neuropathic pain development following nerve injury is mediated by SOX11-ARID1A-SOCS3 transcriptional regulation in the spinal cord.Molecular biology reports · 2024Article
- Targeting the JAK2/STAT3 signaling pathway for chronic pain.Aging and disease · 2024Review
- Expression of NF-κB-associated lncRNAs in different types of migraine.Acta neurologica Belgica · 2023Article
- Research progress on long non-coding RNAs for spinal cord injury.Journal of orthopaedic surgery and research · 2023Review
- The emerging power and promise of non-coding RNAs in chronic pain.Frontiers in molecular neuroscience · 2022Review
- Transcriptomic Analysis of Long Noncoding RNA and mRNA Expression Profiles in the Amygdala of Rats with Bone Cancer Pain-Depression Comorbidity.Life (Basel, Switzerland) · 2021Article
- The Expanding Regulatory Mechanisms and Cellular Functions of Long Non-coding RNAs (lncRNAs) in Neuroinflammation.Molecular neurobiology · 2021Review
- The Tyrosine Kinase-Driven Networks of Novel Long Non-coding RNAs and Their Molecular Targets in Myeloproliferative Neoplasms.Frontiers in cell and developmental biology · 2021Article
- Roles of Long Non-coding RNAs in the Development of Chronic Pain.Frontiers in molecular neuroscience · 2021Review
- Promoting functions of microRNA-29a/199B in neurological recovery in rats with spinal cord injury through inhibition of the RGMA/STAT3 axis.Journal of orthopaedic surgery and research · 2020Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long noncoding RNAs (lncRNAs) have been involved in the development of multiple pathological processes including neuropathic pain. The aim of the present study is to investigate the role of lncRNA down-regulated in liver cancer stem cells (DILC) in the progression of neuropathic pain and its underlying mechanism. Neuropathic pain rat model was established with the bilateral chronic constriction injury (bCCI) method. The results from quantitative PCR analysis in the spinal cord showed that DILC was significantly up-regulated in rats with bCCI compared with the sham group. DILC down-regulation mediated by intrathecal administration of DILC siRNA significantly increased the mechanical shrinkage threshold (MWT) and paw withdrawal threshold latency (PWTL), decreased the positive frequency for nerve sensitivity to cold and suppressed the expression of inflammatory genes in bCCI rats. Down-regulation of DILC induced suppressor of cytokine signaling (SOCS3) expression and inhibited the phosphorylation of signal transducer and activator of transcription 3 (p-STAT3) in spinal cord tissues. Western blotting showed that down-regulation of DILC by DILC siRNA transfection induced SOCS3 expression and inhibited the expression of p-Janus kinase 2 (p-JAK2) and p-STAT3 and their downstream genes in primary microglia. Furthermore, down-regulation of DILC increased the viability of primary microglia, suppressed apoptosis, and inhibited the production of interleukin (IL)-6 and IL-1β in microglia. In contrast, overexpression of DILC showed the opposite functions to those of DILC knockdown. In conclusion, silence of lncRNA DILC attenuates neuropathic pain via SOCS3-induced suppression of the JAK2/STAT3 pathway.
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