| Arteriosclerosis (AS) is a pathological basis of many cardiovascular diseases. The pathogenesis of AS is very complicated and closely linked to environmental and genetic factors. With the application of molecular biological technique, the pathogenesis of AS became more clear than before. Studies showed that endothelium dysfunction might be a key factor to AS since it often occurs before AS. The endothelium localizes between blood and vessel as barrier, signal sensor and transducer. Endothelial cells produce and secrete many factors, which take part in many important physiological procedures to maintain the balance between coagulation and anticoagulation, or vessel contraction and relaxation and so on. The endothelium is the major sites for PAI-1 production (plasminogen activator inhibitor-1, PAI-1) . It was known that PAI-1 belongs to serine protein kinase inhibitor super family and is important regulator in fibrinolysis system since it can inhibit plasminogen activator. The abnormal expression of PAI-1 is closely associated to thrombotic diseases. PAI-1 level increases in blood of AS patient, and the PAI-1 mRNA level in vessel with severe AS plaque is more than normal vessel. These results suggested that the high expression of PAI-1 might lead to result to the decease of fibrinolysis function in AS patients. Studies also showed that PAI-1 expression was increased when endothelial dysfunction occurred. It seems that abnormal expression of PAI-1 in dysfunctional endothelium may be one of pathogenesis of AS.TNF-α Tumor Necrosis Factor α , TNF-α ) or mmLDL (minimal modified low density lipoprotein, mmLDL) are two risk factors of AS. It was reported that TNF- α or oxLDL could induce PAI-1 abnormal expression in endothelium, but there is no report about mmLDL inducting PAI-1 gene expression, and the signal transduction and the role of PAI-1 promoter in PAI-1 expression still remained unclear yet. The aim of this study is...
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