miR‐98 acts as an inhibitor in chronic constriction injury‐induced neuropathic pain via downregulation of high‐mobility group AT‐hook 2

Neuropathic pain, resulting from somatosensory nervous system dysfunction, remains a serious public health problem worldwide. microRNAs are involved in the physiological processes of neuropathic pain. However, the biological roles of miR‐98 in neuropathic pain development have not been investigated. Therefore, in our current study, we focused on the effects of miR‐98 in neuropathic pain. It was shown that miR‐98 was significantly downregulated in chronic sciatic nerve injury (CCI) rat models. In addition, high mobility group A2 (HMGA2) was obviously upregulated in CCI rats. Overexpression of miR‐98 inhibited neuropathic pain progression, including mechanical and thermal hyperalgesia. By a bioinformatics analysis, HMGA2 was predicted as a direct target of miR‐98. The negative correlation between miR‐98 and HMGA2 was validated in our present study. Furthermore, overexpression of miR‐98 dramatically repressed HMGA2 protein and messenger RNA (mRNA) expression. Neuroinflammation participates in neural‐immune interactions, which can contribute to the neuropathic pain development. Meanwhile, we found that inflammatory cytokine (interleukin [IL]‐6, IL‐1β, and COX‐2) protein expression in rats infected with LV‐miR‐98 was greatly suppressed. Taking these results together, we concluded that miR‐98 might depress neuropathic pain development through modulating HMGA2. We found that miR‐98 was able to alleviate neuropathic pain progression in chronic sciatic nerve injury (CCI) rats via targeting the high mobility group A2 (HMGA2). Apart from this, miR‐98 overexpression inhibited neuroinflammation by reducing interleukin (IL)‐6, IL‐1β, and COX‐2. We reported that miR‐98 alleviated neuropathic pain development via targeting HMGA2.