miR-362-3p Knockdown Triggers Inflammation to Promote Neuropathic Pain by Modulating JMJD1A Expression

Objective: When nerve injury or inflammatory injury, different miRNA-mediated signal pathways are activated or inactivated, causing pain or hyperalgesia. Therefore, miRNA has become a new direction of pain mechanism research. We aimed to investigate the effect and mechanism of miR-362-3p on neuropathic pain in rats with chronic sciatic nerve injury (CCI). Methods: Neuropathic pain CCI rat model was established. Real-time-quantitative polymerase chain reaction (RT-PCR), Western blot, immunofluorescence, intrathecal injection, Enzyme-linked immunosorbent assay (ELISA), and dual luciferase reporter gene assays were used to explore the role of miR-362-3p in neuropathic pain development and the relationship between miR-362-3p and JMJD1A (Jumonji domain-containing 1A). Results: In the CCI group, the miR-362-3p level was increased and JMJD1A level was reduced in spinal cords and isolated microglia. The paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) values were increased, the secretion of inflammatory factors was reduced, and the microglial marker Iba1 expression was decreased after intrathecal administration of miR-362-3p. miR-362-3p was observed to target JMJD1A. JMJD1A elevation abolished the inhibitory effects of miR-362-3p on neuropathic pain development. Conclusion: Intrathecal administration of miR-362-3p significantly relieved neuropathic pain in CCI rats and inhibited neuroinflammation possibly through regulating JMJD1A.