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Long non-coding RNA Mirt2 relieves lipopolysaccharide-induced injury in PC12 cells by suppressing miR-429.
Journal of Physiology and Biochemistry ( IF 3.4 ) Pub Date : 2019-07-15 , DOI: 10.1007/s13105-019-00691-7
Haibo Li 1 , Yu Xu 1 , Guoxiu Wang 2 , Xuerong Chen 1 , Wenqing Liang 1 , Huawei Ni 3
Affiliation  

Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) play important roles in the pathogenesis of spinal cord injury (SCI). This study investigated the effects of lncRNA Mirt2 and miR-429 on lipopolysaccharide (LPS)-induced injuries in PC12 cells. Serum samples were collected from 36 patients with SCI and the healthy controls. The expression of lncRNA Mirt2 in serum samples was measured by qRT-PCR. The in vitro model of SCI was established by treating PC12 cells with LPS. The effects of lncRNA Mirt2 and miR-429 on the cell model were evaluated by CCK-8 assay, flow cytometry, western blot, qRT-PCR, and ELISA. Further, the activation of NF-κB and p38MAPK pathways was tested by western blot. LPS induced obvious cell injuries in PC12 cells, as cell viability was reduced, apoptosis rate was increased, caspase-3 and -9 were cleaved, and the release of TNF-α and IL-6 was induced. lncRNA Mirt2 was up-regulated in LPS-stimulated PC12 cells and serum samples derived from SCI patients. Overexpression of lncRNA Mirt2 protected PC12 cells against LPS-induced injuries. Further studies found that lncRNA Mirt2 acted as the molecular sponge of miR-429 and miR-34a-5p. lncRNA Mirt2 did not protect PC12 cells when miR-429 was overexpressed. Moreover, the inhibitory effects of lncRNA Mirt2 on NF-κB and p38MAPK pathways were abolished when miR-429 was overexpressed. lncRNA Mirt2 exerts protective effects in an in vitro model of SCI by down-regulating miR-429. This study shed light on the treatment of SCI by using the lncRNA-miRNA regulation network.

中文翻译:

长链非编码 RNA Mirt2 通过抑制 miR-429 减轻脂多糖诱导的 PC12 细胞损伤。

长链非编码 RNA (lncRNAs) 和 microRNAs (miRNAs) 在脊髓损伤 (SCI) 的发病机制中发挥重要作用。本研究调查了 lncRNA Mirt2 和 miR-429 对脂多糖 (LPS) 诱导的 PC12 细胞损伤的影响。从 36 名 SCI 患者和健康对照组收集血清样本。通过qRT-PCR测量血清样品中lncRNA Mirt2的表达。用LPS处理PC12细胞建立SCI体外模型。通过CCK-8测定、流式细胞术、蛋白质印迹、qRT-PCR和ELISA评估lncRNA Mirt2和miR-429对细胞模型的影响。此外,通过蛋白质印迹测试了 NF-κB 和 p38MAPK 通路的激活。LPS对PC12细胞造成明显的细胞损伤,细胞活力降低,凋亡率增加,caspase-3和-9被裂解,并诱导TNF-α和IL-6的释放。lncRNA Mirt2 在 LPS 刺激的 PC12 细胞和来自 SCI 患者的血清样本中上调。lncRNA Mirt2的过表达保护PC12细胞免受LPS诱导的损伤。进一步研究发现,lncRNA Mirt2充当了miR-429和miR-34a-5p的分子海绵。当 miR-429 过表达时,lncRNA Mirt2 不能保护 PC12 细胞。此外,当 miR-429 过表达时,lncRNA Mirt2 对 NF-κB 和 p38MAPK 通路的抑制作用被消除。lncRNA Mirt2通过下调miR-429在SCI体外模型中发挥保护作用。本研究阐明了使用 lncRNA-miRNA 调控网络治疗 SCI。lncRNA Mirt2的过表达保护PC12细胞免受LPS诱导的损伤。进一步研究发现,lncRNA Mirt2充当了miR-429和miR-34a-5p的分子海绵。当 miR-429 过表达时,lncRNA Mirt2 不能保护 PC12 细胞。此外,当 miR-429 过表达时,lncRNA Mirt2 对 NF-κB 和 p38MAPK 通路的抑制作用被消除。lncRNA Mirt2通过下调miR-429在SCI体外模型中发挥保护作用。本研究阐明了使用 lncRNA-miRNA 调控网络治疗 SCI。lncRNA Mirt2的过表达保护PC12细胞免受LPS诱导的损伤。进一步研究发现,lncRNA Mirt2充当了miR-429和miR-34a-5p的分子海绵。当 miR-429 过表达时,lncRNA Mirt2 不能保护 PC12 细胞。此外,当 miR-429 过表达时,lncRNA Mirt2 对 NF-κB 和 p38MAPK 通路的抑制作用被消除。lncRNA Mirt2通过下调miR-429在SCI体外模型中发挥保护作用。本研究阐明了使用 lncRNA-miRNA 调控网络治疗 SCI。当 miR-429 过表达时,lncRNA Mirt2 对 NF-κB 和 p38MAPK 通路的抑制作用被消除。lncRNA Mirt2通过下调miR-429在SCI体外模型中发挥保护作用。本研究阐明了使用 lncRNA-miRNA 调控网络治疗 SCI。当 miR-429 过表达时,lncRNA Mirt2 对 NF-κB 和 p38MAPK 通路的抑制作用被消除。lncRNA Mirt2通过下调miR-429在SCI体外模型中发挥保护作用。本研究阐明了使用 lncRNA-miRNA 调控网络治疗 SCI。
更新日期:2019-07-15
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