Study On The Function Of MiR-155 In The Regulation Of Endothelial Cell Through Autophagy Under Oxidative Stress

Objective:Now,the morbidity of coronary heart disease,hypertension and other chronic vascular disease increased year by year,prevention and control work is extremely important.Endothelial cells dysfunction is an important basic pathological for the development of vascular disease.Intravascular lipid metabolism disorders,hypoxia and other causes of endothelial cell injured,the barrier between blood and vessels was weakened,induced platelet aggregation,vasospasm,thrombosis,vascular stenosis.Therefore,the protection and maintenance of the normal function of vascular endothelial cells,promote the proliferation of endothelial cells and improve cell viability is the focus on chronic injury of vascular disease in current.MicroRNA(mirco RNA)is a typical multifunctional non-coding RNA that degrades or inhibits expression of mRNA at the transcriptional level and regulates cell function.Its related with cell generation,inflammation,tumor development and other pathophysiology.Autophagy is a protective procedure in cells that capable to digested and degraded injury organelles to maintain intracellular environmental homeostasis.MicroRNAs effected the development and progression of atherosclerosis by autophagy have been reported,but less research has been done on the role of miR-155 in injured endothelial cells.This study aim to explored the effects of miR-155 on injured endothelial cells under oxidative stress and its possible regulatory mechanism.Method:1、We purchased Human umbilical vein endothelial cells from Sicence cells bank.The hydrogen peroxide was used to duplication oxidative stress injury cells model.The cells model was identified by detect the production of reactive oxygenspecies(ROS)and the degree of autophagy.2、In the oxidative stress injured cells model,we used plasmidto transfected miR-155,Then monitor the effect on the production of cytotoxicity substance ROS and the proliferation of endothelial cells.Also we used the Western Blotting,Revserse transcription-quantitative polymerase chain reaction(RT-qPCR)and copolymerization immunofluorescence to detect the level of autophagy.3、Explore the function of ATG5 in miR-155 regulated the dysfunction endothelial cells.Results:1、The suitable concentration and time point of H2O2 pretreatment to endothelial cells was 400nmol/l at 12h.It the suitable condition to establish oxidative stress injury cell models which the production of cytotoxicity substance ROS was get smoothy and the level of autophagy was the highest.2.Inhibitor the expression of miR-155 can promoted the degree of autophagy in injury endothelial cells and decreased the production of cytotoxicity substance ROS,the ability of proliferation was also increased.3、We fund that regulated the expression of ATG5 can effected the degree of autophagy in injured endothelial cells after transfected miR-155.Conclusion:miR-155 can reduce the production of cytotoxic substances ROS,improve the survival rate of damaged endothelial cells under oxidative stress by autophagy;among them,the function of autophagy regulation may be achieved through the ATG5 pathway.