MicroRNAs (miRNAs) have been shown to participate in development of neuropathic pain. However, the role of microRNA-144 (miR-144) in neuropathic pain remains unclear. In the present study, we established a neuropathic pain mouse model via chronic constriction injury (CCI)-induction. The successful establishment of this model was confirmed via evaluation of paw withdrawal threshold (PWT) and paw withdrawal latency (PWL). By using this model, we found that miR-144 was significantly downregulated in CCI-induced neuropathic pain mice. In addition, intrathecal injection of miR-144 agomiR alleviated mechanical and thermal hyperalgesia in neuropathic pain mice as shown by the increased of PWT and PWL. Moreover, miR-144 negatively regulated neuroinflammation by decreasing the expression of proinflammatory mediators, including TNF-α (tumor necrosis factor-α), IL (interleukin)-1β, and IL-6, thus facilitating the inhibition of neuropathic pain development. Mechanistically, RASA1 (RAS P21 Protein Activator 1) was downregulated following the injection of agomiR-144, and was verified to be a target of miR-144. Furthermore, overexpression of RASA1 reversed the inhibitory effect of miR-144 on neuropathic pain. Therefore, the present study suggested that miR-144 has the potential to be explored as therapeutic target for treatment of neuropathic pain.
Keywords: RASA1; miR-144; neuroinflammation; neuropathic pain.
© 2019 International Union of Biochemistry and Molecular Biology, Inc.