摘要
目的研究过表达miR-338-3p在内皮细胞系EOMA中对炎症信号通路的影响。方法将EOMA细胞分为四组即对照组、miR-338-3p过表达组、TNF-α处理组、miR-338-3p与TNF-α共处理组。用Real time PCR检测miR-338-3p及黏附分子VCAM-1和ICAM-1mRNA表达水平,Western blot分析ERK/p38 MAPK信号通路活性。结果与对照组比较,miR-338-3p过表达组的黏附分子VCAM-1及ICAM-1mRNA表达水平和ERK/p38信号通路活性明显降低,而TNF-α处理组的黏附分子VCAM-1及ICAM-1mRNA表达水平和ERK/p38信号通路活性明显升高;miR-338-3p与TNF-α共处理组与TNF-α处理组比较,黏附分子VCAM-1及ICAM-1mRNA表达水平和ERK/p38信号通路活性明显降低;miR-338-3p与TNF-α共处理组与miR-338-3p过表达组比较,黏附分子表达水平及ERK/p38信号通路活性不再升高。结论过表达miR-338-3p抑制ERK/p38信号通路活性,降低黏附分子VCAM-1和ICAM-1mRNA表达水平;过表达miR-338-3p能够逆转TNF-α对ERK/p38通路的激活和TNF-α对黏附分子VCAM-1及ICAM-1mRNA表达的促进作用。
Objective Aims Our studyaims toinvestigate the effect of miR-338-3p on the inflammatory signal pathway in endothelial cell line EOMA. Methods EOMA cells were divided into four groups:control group,miR-338-3p over expression group,TNF-α treatment group,miR-338-3p and TNF-α treatment. Results Compared with the control group,miR-338-3p over expression group of adhesion molecule VCAM-1 and ICAM-1 expression level of mRNA and ERK/p38 signaling pathway activity decreased significantly,and TNF-α treatment group of adhesion molecule VCAM- 1 and ICAM-1 expression level of mRNA and ERK/p38 signaling pathway activity was significantly increased; miR- 338-3p and TNF-α treated group compared with TNF-α treatment,adhesion molecule VCAM-1 and ICAM-1 expression of mRNA was significantly reduced,ERK/p38 pathway activity decreased significantly; miR-338-3p and TNF-α treated group and tniR-338-3p overexpression group,adhesion molecule expression and ERK/p38 signaling pathway activity is no longer increasing. Conclusion Overexpression of miR-338-3p inhibited the activation of ERK and p38 signal pathways and reduced the levels of VCAM-1 and ICAM-1. Overexpression of miR-338-ap can reverse the effect of TNF-α on the activation of ERK/p38 pathway and the promotion of the expression of VCAM-1 and ICAM-1.
出处
《中国实验诊断学》
2017年第11期1991-1995,共5页
Chinese Journal of Laboratory Diagnosis
基金
黑龙江省教育厅科学技术研究项目(2016-KYYWF-0593)