MiR‑15a attenuates peripheral nerve injury‑induced neuropathic pain by targeting AKT3 to regulate autophagy

Longxue Cai; Xianfa Liu; Qicai Guo; Qi huang; Qiong Zhang; Zuohong Cao

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자료유형: 학술저널

저자정보: Longxue Cai (First Affiliated Hospital of Gannan Medical University) Xianfa Liu (First Affiliated Hospital of Gannan Medical University) Qicai Guo (First Affiliated Hospital of Gannan Medical University) Qi huang (First Affiliated Hospital of Gannan Medical University) Qiong Zhang (First Affiliated Hospital of Gannan Medical University) Zuohong Cao (First Affiliated Hospital of Gannan Medical University)

저널정보: 한국유전학회 Genes & Genomics Genes & Genomics Vol.42 No.1

발행연도: 2020.1

수록면: 77 - 85 (9page)

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Objective Aim of this study was to detect the expression of miR-15a in rats following chronic constriction injury (CCI) and to investigate the regulatory functions of miR-15a during neuropathic pain (NP) development. Methods CCI was performed in adult Sprague–Dawley rats to set up the rat model of neuropathic pain. MiR-15a agomir and scrambled control were delivered into the implanted catheter of rats. The mechanical allodynia and thermal hyperalgesia were assessed in both CCI- and sham-operated groups. Rat lumbar spinal cord tissues were harvested for mRNA and protein analyses. The primary spinal microglia were isolated from adult Sprague–Dawley rats and transfected with miR-15a mimics, scramble miRNA, miR-15a inhibitor or its corresponding negative control. Cell lysates were collected for mRNA and protein analyses. Results Compared to sham-operated group, the expression of miR-15a in CCI rats was significantly reduced, whereas neuroinflammation in spinal cord tissues was increased. Intrathecal administration of miR-15a agomir significantly attenuated CCI-induced NP and the levels of proinflammatory cytokines, including IL-6, IL-1β, and TNF-α. AKT3 was predicted and confirmed as a miR-15a-regulated gene. We further demonstrated that miR-15a overexpression downregulated the level of AKT3 in primary rat microglia and rat CCI model. Moreover, the upregulation of miR-15a induced the expressions of autophagy-associated proteins, suggesting that the regulation mechanism of miR-15a in NP development involves AKT3mediated autophagy via inhibiting the expression of AKT3. Conclusion Our findings indicated that miR-15a might serve as a promising therapeutic target for the management of NP through the stimulation of autophagic process.

#AKT3 · Autophagy · Chronic constriction injury · miR-15a · Neuropathic pain

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