Chen Huifen, Liu Gao Mi Yang, Zhang Li, He Fa Lian, Shi Yan Kun, Pan Xing Hua, Wang Hong
Department of Cardiology, Hengyang Central Hospital, Hengyang, Hunan 421000, P.R. China.
Department of Clinical Experiment, Kunming General Hospital, Kunming, Yunnan 650032, P.R. China.
Oncol Lett. 2019 Feb;17(2):2237-2243. doi: 10.3892/ol.2018.9860. Epub 2018 Dec 21.
MicroRNA-155 (miRNA-155) is a typical multifunctional miRNA, which serves a crucial role in the regulation of numerous vessel cells. However, its effects on dysfunctional endothelial cells have not been completely elucidated. In order to investigate the signaling pathway of miRNA-155-induced cell injury, HO was used to establish an oxidative stress cell model, and miR-155 was transfected into HO-treated cells. The CCK8 assay was then employed to examine the effect of miR-155 on the cell proliferations of HOtreated cells, and the expressions of Microtubule Associated Protein 1 Light Chain 3 (LC3) and Sequestosome 1 (P62) were detected to examine the effect of miR-155 on the autophagy of , and then the formation of intracellular autophagosomes was observed. The results indicated that endothelial cell proliferation was promoted, and oxidant-induced injury was decreased when the expression of miR-155 was inhibited. In addition, the results also demonstrated that when the miR-155 inhibitor was used, the expression of LC3 was increased and the expression of P62 was decreased. This suggests that modulated miR-155 can prevent oxidative damage in endothelial cells, by regulating the level of autophagy. Furthermore, the present study also demonstrated that miR-155 regulated autophagy via promotion of the expression of the autophagy-related gene, Autophagy Related 5 (). In conclusion, the attenuated expression of miR-155 can decrease oxidant-induced injury and promote cell proliferation via upregulating autophagy, which subsequently affects the expression of ATG5. The present study provides a novel insight into microRNAs as potential therapeutics for the treatment of heart disease.
微小RNA-155（miRNA-155）是一种典型的多功能微小RNA，在多种血管细胞的调节中起关键作用。然而，其对功能失调的内皮细胞的影响尚未完全阐明。为了研究miRNA-155诱导细胞损伤的信号通路，利用过氧化氢（HO）建立氧化应激细胞模型，并将miR-155转染到经HO处理的细胞中。然后采用CCK8法检测miR-155对经HO处理细胞的细胞增殖的影响，并检测微管相关蛋白1轻链3（LC3）和聚集体蛋白1（P62）的表达，以检测miR-155对自噬的影响，随后观察细胞内自噬体的形成。结果表明，抑制miR-155的表达可促进内皮细胞增殖，并减少氧化剂诱导的损伤。此外，结果还表明，使用miR-155抑制剂时，LC3的表达增加而P62的表达减少。这表明调节miR-155可通过调节自噬水平来预防内皮细胞的氧化损伤。此外，本研究还表明，miR-155通过促进自噬相关基因自噬相关5（ATG5）的表达来调节自噬。总之，miR-155表达减弱可通过上调自噬来减少氧化剂诱导的损伤并促进细胞增殖，进而影响ATG5的表达。本研究为微小RNA作为治疗心脏病的潜在疗法提供了新的见解。
