Injury of endothelial cells has been assumed to be an initial trigger of the development of @entity731 . In this study, we investigated the molecular mechanisms of endothelial cell death induced by @entity519 , which leads to oxidative stress. To study the relation between @entity519 -induced cell death and activation of @entity2451 ( @entity2451 ) in a @entity519 state, we evaluated the effect of 2 antioxidant drugs, @entity5119 and @entity13373 ( @entity14568 ), on @entity1 endothelial apoptosis. Although @entity519 treatment of @entity1 aortic endothelial cells resulted in a significant decrease in cell number and a significant increase in apoptotic cells compared with that of cells under normoxia (P<0.01), treatment with @entity5119 (50 micromol/L) or @entity14568 (100 micromol/L) significantly attenuated the decrease in cell number (P<0.01) and was accompanied by inhibition of @entity2451 activation. Furthermore, downregulation of @entity588 caused by @entity519 was inhibited by these drugs. We further investigated the translocation of @entity589 protein from the cytoplasm to the mitochondrial heavy fraction membrane, as translocation of @entity589 protein is considered to be a determinant of apoptosis. Interestingly, we found that antioxidant treatment inhibited the translocation of @entity589 protein caused by @entity519 . Moreover, upregulation of @entity876 , a proapoptotic molecule, was observed in @entity519 , whereas treatment with @entity5119 attenuated the expression of @entity876 accompanied by suppression of @entity2451 activation. These data suggest functional links between @entity876 and endothelial apoptosis through the activation of @entity2451 . Overall, the current study demonstrated that oxidative stress induced apoptosis in @entity1 aortic endothelial cells through the downregulation of @entity588 , translocation of @entity589 , and upregulation of @entity876 , probably through @entity2451 activation. Oxidative stress may play an important role in endothelial apoptosis mediated by @entity519 , through the activation of @entity2451 .

Endothelial apoptosis induced by oxidative stress through activation of XXXX : antiapoptotic effect of antioxidant agents on endothelial cells.

@entity1 :: ('9606', 'Species') :: ['human'] @entity589 :: ('581', 'Gene') :: ['bax'] @entity2451 :: ('4790', 'Gene') :: ['nuclear factor-kappaB', 'NF-kappaB'] @entity588 :: ('596', 'Gene') :: ['bcl-2'] @entity13373 :: ('MESH:C020972', 'Chemical') :: ['pyrrolidine dithiocarbamate'] @entity876 :: ('7157', 'Gene') :: ['p53'] @entity519 :: ('MESH:D000860', 'Disease') :: ['hypoxic', 'hypoxia'] @entity5119 :: ('MESH:D011341', 'Chemical') :: ['probucol'] @entity14568 :: ('MESH:C066229', 'Chemical') :: ['PDTC'] @entity731 :: ('MESH:D050197', 'Disease') :: ['atherosclerosis']
@entity2451 :: (4790,Gene) :: ['NF-kappaB']
