Myeloreroxidase Induces Apioptosis Of Endothelial Cells In Vitro

Objective: Endothelial cell impairment is the initial stage of atherosclerosis. Both domestic and international studies have confirmed that the focal endothelial cell impairment and its functional disorder are correlated to the severity of the angina pectoris. Aggravation of endothelial cell impairment might be the pathological and physiological foundation for deteriorating of illness and ACS. It is surmised that endothelial impairment and endothelial dysfunctions have great impact on the thrombogenesis of endothelial erosion on eroded plaque. Recently it was demonstrated that an increased MPO level in patient's blood serves as a risk marker for atherosclerosis and coronary artery disease. Recent researches found MPO to be directly linked to the development of atherosclerosis. The latest investigations reported the potential role of MPO in the progressive formation of atherosclerotic plaque and it can be the target molecule for new drug development. Furthermore MPO serum level reflects the dysfunction of endothelial cells and oxidative stress in the atherosclerotic plaque. This study was to investigate the relationship between MPO and endothelial cell proliferation and apoptosis.Method: The First method used is the MTT assay in 0.01-0.2 u/ml concentration range of MPO to assess the EC growth and proliferation. The only concentration of the MPO is 0.1u/ml, which significantly inhibited ECV304 endothelial cell growth and proliferation in vitro. To quantify the apoptotic EC count we used AO/EB stained with fluorescent microscopy and flow cytometry techniques, which demonstrated that MPO in 0.1u/ml concentration could lead to ECV304 EC apoptosis, which was time-dependent.Result: The 0.1u/ml MPO inhibits ECV304 endothelial cells growth and proliferation.The 0.1u/ml MPO induced apoptosis of ECV304 endothelial cells.Conclusion: The MPO triggers inhibition in ECV304 EC growth and proliferation and also induces EC apoptosis in a time-dependent fashion.