CIRCGRIN2B Acts as an Inhibitor in Neuropathic Pain Via Upregulation of Slick
Neuropathic pain, resulting from somatosensory nervous system dysfunction, remains a serious public health problem worldwide. CircRNAs are involved in the physiological processes of neuropathic pain. However, the biological roles of circGRIN2B in neuropathic pain development have not been investigated. Therefore, in our current study, we focused on the effects of circGRIN2B in neuropathic pain. It was shown that circGRIN2B was significantly upregulated in chronic sciatic nerve injury (CCI) rat models. In addition, SLICK was obviously downregulated in CCI rats. Overexpression of circGRIN2B inhibited neuropathic pain progression, including mechanical and thermal hyperalgesia. The positive correlation between circGRIN2B and SLICK was validated in our present study. Furthermore, overexpression of circGRIN2B dramatically repressed SLICK 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 TNF-α) protein expression in rats infected with LV-circGRIN2B was greatly suppressed. Taking these results together, we concluded that circGRIN2B might depress neuropathic pain development through modulating SLICK.
Keywords - Neuropathic Pain, circRNA, SLICK, Inflammatory Cytokine