Regulation by DDAH/ADMA pathway of lipopolysaccharideinduced tissue factor expression in endothelial cells

摘要: Previous studies have shown the regulatory effect of nitric oxide (NO) on endotoxin-induced tissue factor (TF) in endothelial cells. Asymmetric dimethylarginine (ADMA), a major endogenous NO synthase (NOS) inhibitor, could inhibit production vivo and vitro.ADMA its hydrolase dimethylaminohydrolase (DDAH) recently been thought as novel system productionity induced by LPS, whereas L-arginine, NOS substrate, markedly attenuated LPS-induced TF increment. LPS increased level ADMA cultured medium decreased DDAH activity cells, overexpression DDAH2 significantly suppress increment increase intracellular reactive oxygen species (ROS) activate nuclear factor-κB, which were enhanced exogenous either L-arginine or DDAH2. Therefore, our present results for first time suggest that DDAH/ADMA pathway can regulate LPS-inducedTF expression via ROS-nuclear factor-κB-dependent The aim study was to determine whether is involved lipopolysaccharide (LPS) Human umbilical vein cells (HUVECs) treated with (1 μg/ml) induce expression. Exogenous both mRNA activ-