a Department of Orthopedics , China-Japan Union Hospital of Jilin University , Changchun , China.
b Department of Anesthesiology , China-Japan Union Hospital of Jilin University , Changchun , China.
Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):1444-1451. doi: 10.1080/21691401.2019.1600530.
Functions of long non-coding RNAs (lncRNAs) have been widely probed in spinal cord injury (SCI). But, the influences of lncRNA-small nucleolar RNA host gene 16 (lncRNA-SNHG16) is still not well documented in SCI. The study explored the impacts of SNHG16 on HO-injured PC-12 cells. PC-12 cells were disposed with HO, cell viability, apoptosis, autophagy and ROS level were detected. RT-qPCR was executed to explore SNHG16 or miR-423-5p expression in HO-stimulated cells. After transfection with pc-SNHG16 or miR-423-5p inhibitor, the functions of SNHG16 and miR-423-5p in HO-injured cells were studied. AMPK and ERK1/2 pathways were finally assessed by western blot. We found that HO evoked cell injury in PC-12 cells, and repressed SNHG16 was observed in HO-disposed cells. Overexpressed SNHG16 prominently alleviated HO-induced cell injury as indicated by repressing cell apoptosis, autophagy and ROS level. Additionally, SNGH16 enhanced miR-423-5p expression, and miR-423-5p inhibition abrogated the protective effect of SNGH16 on HO-injured PC-12 cells. SNGH16 mediated AMPK and ERK1/2 pathways via up-regulating miR-423-5p in HO-injured PC-12 cells. In conclusion, these findings indicated that SNGH16 reduced HO-evoked cell injury by mediating miR-423-5p in PC-12 cells. The findings might uncover the effect of SNHG16 on SCI, which provide a new reference for remedying SCI. Highlights HO evokes cell injury in PC-12 cells; SNHG16 reduces HO-induced cell injury in PC-12 cells; SNGH16 enhances miR-423-5p expression in HO-stimulated PC-12 cells; MiR-423-5p inhibition abrogates the protective effect of SNGH16 in PC-12 cells; SNGH16 mediates AMPK and ERK1/2 pathways by up-regulating miR-423-5p.
长链非编码 RNA（lncRNA）的功能已在脊髓损伤（SCI）中广泛研究。但是，lncRNA-小核仁 RNA 宿主基因 16（lncRNA-SNHG16）在 SCI 中的影响仍未得到很好的证明。本研究探讨了 SNHG16 对 HO 损伤的 PC-12 细胞的影响。用 HO 处理 PC-12 细胞，检测细胞活力、细胞凋亡、自噬和 ROS 水平。执行 RT-qPCR 以探讨 HO 刺激细胞中 SNHG16 或 miR-423-5p 的表达。转染 pc-SNHG16 或 miR-423-5p 抑制剂后，研究 SNHG16 和 miR-423-5p 在 HO 损伤细胞中的功能。最后通过 Western blot 评估 AMPK 和 ERK1/2 通路。我们发现 HO 可引起 PC-12 细胞损伤，并且在 HO 处理的细胞中观察到 SNHG16 的表达下调。过表达 SNHG16 可明显减轻 HO 诱导的细胞损伤，表现为抑制细胞凋亡、自噬和 ROS 水平。此外，SNGH16 增强了 miR-423-5p 的表达，而 miR-423-5p 抑制消除了 SNGH16 对 HO 损伤的 PC-12 细胞的保护作用。SNGH16 通过上调 HO 损伤的 PC-12 细胞中的 miR-423-5p 来介导 AMPK 和 ERK1/2 通路。总之，这些发现表明 SNGH16 通过在 PC-12 细胞中介导 miR-423-5p 来减轻 HO 引起的细胞损伤。这些发现可能揭示了 SNHG16 对 SCI 的影响，为 SCI 的治疗提供了新的参考。
