ArticleGenes & genomics2019
MicroRNA-340-5p relieved chronic constriction injury-induced neuropathic pain by targeting Rap1A in rat model.
Article in Genes & genomics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Neuropathic Pain: Mapping the miRNA Landscape.Non-coding RNA · 2026Review
- Identification of a New Role of miR-199a-5p as Factor Implied in Neuronal Damage: Decreasing the Expression of Its Target X-Linked Anti-Apoptotic Protein (XIAP) After SCI.International journal of molecular sciences · 2024Article
- The role of non-coding RNAs in neuropathic pain.Pflugers Archiv : European journal of physiology · 2024Review
- The emerging power and promise of non-coding RNAs in chronic pain.Frontiers in molecular neuroscience · 2022Review
- Identification of Regeneration and Hub Genes and Pathways at Different Time Points after Spinal Cord Injury.Molecular neurobiology · 2021Article
- New Vistas in microRNA Regulatory Interactome in Neuropathic Pain.Frontiers in pharmacology · 2021Review
- Overexpression of microRNA-340-5p Ameliorates Inflammatory Response and Intracellular Survival ofInfection and drug resistance · 2021Article
- MicroRNAs in the Spinal Microglia Serve Critical Roles in Neuropathic Pain.Molecular neurobiology · 2021Review
- Protective effect of microRNA‑340‑5p against oxygen‑glucose deprivation/reperfusion in PC12 cells through targeting neuronal differentiation 4.Molecular medicine reports · 2020Article
- Dexmedetomidine Attenuates Neuroinflammation In LPS-Stimulated BV2 Microglia Cells Through Upregulation Of miR-340.Drug design, development and therapy · 2019Article
- Mechanism of Incisional Pain: Novel Finding on Long Noncoding RNA XIST/miR-340-5p/RAB1A Axis.ASN neuroArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesNeuropathic pain (NP) is one of the main challenges towards NP syndrome treatment. miR-340-5p exhibit different expression levels in NP models. Its effects on NP remained unclear. The objective of this study was to explore the potential regulation mechanisms of miR-340-5p in NP.
methodsRat model of chronic constriction injury (CCI) was established to induce NP in vivo. NP levels were assessed using mechanical withdrawal threshold (MWT). The inflammation response in CCI rats were determined by HE staining and ELISA assay. The target genes of miR-340-5p were verified by luciferase report assays.
resultsIn CCI rats, level of miR-340-5p was down-regulated both in spinal cord tissues and isolated microglial cells. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were decreased in CCI rats, which were restored upon miR-340-5p overexpression. miR-340-5p overexpression also decreased inflammation as well as expression levels of COX-2, IL-1β, TNF-α and IL-6 in CCI rats. Luciferase report assays revealed Rap1A was a target gene of miR-340-5p in the experimental model. Elevated miR-340-5p decreased Rap1A expression level in vitro and in vivo. Overexpression of Rap1A protein restored expression levels of COX-2, IL-1β, TNF-α and IL-6, reduced the PWT and PWL and increased inflammation response in CCI rats.
conclusionmiR-340-5p alleviated CCI-induced NP by targeting Rap1A. miR-340-5p and Rap1A may be the potential treatment targets for NP therapeutics.
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