MiR-31-5p regulates the neuroinflammatory response via TRAF6 in neuropathic pain
Open Access
- 24 January 2024
- journal article
- research article
- Published by Springer Nature in Biology Direct
- Vol. 19 (1) , 1-16
Abstract
Background: Neuropathic pain is chronic pain and has few effective control strategies. Studies have demonstrated that microRNAs have functions in neuropathic pain. However, no study has been conducted to demonstrate the role and mechanism of microRNA (miR)-31-5p in neuropathic pain. Accordingly, this study sought to determine the pathological role of miR-31-5p in chronic constriction injury (CCI) -induced neuropathic pain mouse models. Methods: We used CCI surgery to establish mouse neuropathic pain model. Behavioral tests were performed to evaluate pain sensitivity of mice. Expressions of miR-31-5p and inflammatory cytokines in dorsal root ganglion (DRG) were examined by polymerase chain reaction. Animals or cells were received with/without miR-31-5p mimic or inhibitor to investigate its role in neuropathic pain. The mechanism of miR-31-5p was assayed using western blotting, immunofluorescence staining and dual-luciferase reporter assay. Results: We found that CCI led to a significant decrease in miR-31-5p levels. Knockout of miR-31-5p and administration of miPEP31 exacerbated pain in C57BL/6 mice. Meanwhile, miR-31-5p overexpression increased the paw withdrawal threshold and latency. TRAF6 is one of the target gene of miR-31-5p, which can trigger a complex inflammatory response. TRAF6 was associated with pain and that reducing the DRG expression of TRAF6 could alleviate pain. In addition, miR-31-5p overexpression inhibited the TRAF6 expression and reduced the neuroinflammatory response. Conclusions: All the results reveal that miR-31-5p could potentially alleviate pain in CCI mouse models by inhibiting the TRAF6 mediated neuroinflammatory response. MiR-31-5p upregulation is highlighted here as new target for CCI treatment.Keywords
Funding Information
- The National Natural Science Foundation of China (82001178, 82001175, 81901129)
- Shanghai Sailing Program (20YF1439200)
- The Natural Science Foundation of Shanghai, China (23ZR1450800)
This publication has 49 references indexed in Scilit:
- Neuropathic pain in the general population: A systematic review of epidemiological studiesPain, 2014
- Differential expression of rat hippocampal microRNAs in two rat models of chronic painInternational Journal of Molecular Medicine, 2013
- Treatment with Carbon Monoxide-releasing Molecules and an HO-1 Inducer Enhances the Effects and Expression of µ-Opioid Receptors during Neuropathic PainAnesthesiology, 2013
- Increased Expression of TNF Receptor-Associated Factor 6 After Rat Traumatic Brain InjuryCellular and Molecular Neurobiology, 2010
- Neuropathic pain: diagnosis, pathophysiological mechanisms, and treatmentThe Lancet Neurology, 2010
- Types and Epidemiology of Cancer-Related Neuropathic Pain: The Intersection of Cancer Pain and Neuropathic PainThe Oncologist, 2010
- Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural PlasticityThe Journal of Pain, 2009
- Proteomics in Neuropathic Pain ResearchAnesthesiology, 2008
- ERK is sequentially activated in neurons, microglia, and astrocytes by spinal nerve ligation and contributes to mechanical allodynia in this neuropathic pain modelPain, 2005
- TRAF6, a molecular bridge spanning adaptive immunity, innate immunity and osteoimmunologyBioEssays, 2003