期刊文献+

过表达miR-338-3p对炎症信号通路的影响 被引量:2

The effect of overexpression of miR-338-3p on the inflammatory signal pathway
下载PDF
导出
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)
关键词 miR-338-3p 内皮细胞 EOMA TNF-Α 炎症 miR-338-3p endothelial cell EOMA TNF-α inflammatory response
  • 相关文献

参考文献1

二级参考文献9

  • 1Ruiz, M. A. , Chakrabarti, s.. MicroRNAs: The Underlying Medi- ators of Pathogenetic Processes in Vascular Complications of Dia- betes[J]. Can J Diabetes,2013.37(5) :p. 399.
  • 2Osorio-Fuentealba C,Contreras-Ferrat A E, Altamirano F, et al. Electrical stimuli release ATP to increase GLUT4 translocation and glucose uptake via PI3 Kγ-Akt-AS160 in skeletal muscle cells [J]. Diabetes,2013,62(5) : 1519.
  • 3Pogribny,I. P. and Beland,F. A. ,Role of microRNAs in the regu- lation of drug metabolism and disposition genes in diabetes and liver disease[J]. Expert Opin Drug Metab Toxieol,2013.9(6) : p. 713.
  • 4SIMON P R ROMAINE, MACIEJ TOMASZEWSKI,GIANLUI GI CONDORELLI,et al. MicroRNAs in cardiovascular disease:an introduction for clinicians. Heart. 2015,101 : 921-928.
  • 5Guo J, Li M, Meng XY, etal. MiR-291b 3p induces apoptosis in liver cell line NCTC1469 by reducing the level of RNA-binding protein HuR[J]. Cell Physiol Biochem. 2014,33 : 810.
  • 6Zheng,G. X. , et al. A latent pro-survival function for the mir 290- 295 cluster in mouse embryonic stem cells[J]. PLoS Genet,2011. 7(5) :p. e1002054.
  • 7王华,陆玮新,刘凤静,冯波.糖耐量正常的冠心病患者胰岛素抵抗与冠脉病变程度的关系[J].同济大学学报(医学版),2011,32(6):44-47. 被引量:2
  • 8马兰,张基昌,崔燕,武军铎,崔晓倩,杨金英,尚怡君.MicroRNAs与冠心病发生发展关系的研究进展[J].中国实验诊断学,2013,17(7):1354-1357. 被引量:12
  • 9赵潇然,张凤如.心肌再灌注损伤的机制与治疗策略[J].国际心血管病杂志,2014,41(3):158-160. 被引量:14

共引文献1

同被引文献19

引证文献2

二级引证文献6

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部