Upregulation of miR‐22‐3p Alleviates Hyperalgesia and Neuroinflammation Caused by Migraine

作者：Lijun Yang, Feng Li, Linlin Guo, Sihua Qi, Pengcheng Liu · 发表于：Synapse · 年份：2025 · DOI：10.1002/syn.70017 · 被引用次数：4 · 研究领域：Migraine and Headache Studies、Cerebrovascular and genetic disorders、Neuroinflammation and Neurodegeneration Mechanisms

OBJECTIVE: Migraines profoundly impact patients' quality of life. This study seeks to investigate the relationship between dysregulated miR-22-3p and the neuroinflammation and central sensitization associated with migraine. METHODS: Initially, the level of miR-22-3p in migraine patients were analyzed using RT-qPCR. Subsequently, a migraine model was established by administering nitroglycerin (NTG) to mice. To modulate the levels of miR-22-3p within this model, agomir was utilized. Following this intervention, mechanical and thermal pain sensitivity were evaluated by Von Frey filament and radiant heat. The levels of c-Fos, CGRP, TNF-α, IL-1β, and IL-6 in trigeminal nucleus caudalis (TNC) were detected by RT-qPCR and ELISA. Furthermore, dual luciferase reporting assays were conducted to ascertain whether miR-22-3p could target KLF6. Moreover, the influence of KLF6 on inflammatory cytokines and central sensitization were further studied. RESULTS: miR-22-3p was significantly reduced in migraine patients and NTG mice. In animals, overexpression of miR-22-3p significantly alleviated hyperalgesia and neuroinflammation induced by NTG. Following the overexpression of miR-22-3p, we observed an increase in thermal withdrawal latency, paw mechanical threshold, and periorbital mechanical threshold. Conversely, levels of c-Fos, CGRP, TNF-α, IL-1β, and IL-6 exhibited a significant reduction. We found that miR-22-3p can inhibit KLF6 expression. Additionally, further findings indicated that t...