Abstract
Oxidized low-density lipoproteins have a strong cytotoxic effect on cultured endothelial cells that can result in massive apoptosis. We studied the characteristics and mechanism of an effect of an angiotensin-converting enzyme (ACE) inhibitor against oxysterol-induced apoptosis in human aortic endothelial cells. Low concentrations of oxysterols increased apoptosis, but not necrosis. An ACE inhibitor, temocaprilat, significantly and dose-dependently decreased this apoptosis. Addition of HOE 140, a kinin B2 receptor antagonist, or N-nitro-L-arginine methylester (L-NAME), a nitric oxide synthase inhibitor, countered this effect of temocaprilat. The ACE inhibitor lessened increases in caspase-3 activity and intracellular oxygen radical production induced by oxysterols; again, the amelioration was blocked by HOE140 or L-NAME. These findings demonstrate that oxysterols caused endothelial apoptosis via an increase in intracellular reactive oxygen species and activation of caspase-3. Temocaprilat ameliorated apoptosis through increase of nitric oxide production via an increase in bradykinin, with a resulting increase in nitric oxide.
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