Lack of effect of α-tocopherol on in vitro angiogenesis

Oxidative stress and angiogenesis are important elements in the pathogenesis of atherosclerosis and cancer. Because of its antioxidant properties, α-tocopherol has long proposed as prevention of diseases associated with oxidative stress.We explore whether α-tocopherol modulates some cell responses induced by angiogenic and proliferative stimuli. For this purpose, we evaluate the effect in human vein endothelial cells (HUVECs), of α-tocopherol treatment (5–40 μmol/L) for 72 h on the production of reactive oxygen species (ROS), induction of matrix metalloproteinases (MMPs), expression of vascular endothelial–cadherin (VE-cadherin) and α2-integrin, cell migration, cell proliferation, and tube formation.α-Tocopherol significantly inhibits intracellular ROS production induced by TNF-α (P < 0.01) or PMA (P < 0.001). However, α-tocopherol does not interfere with mRNA expression of VE-cadherin, α2-integrin, MMP-1, MMP-2, and MMP-9. Similarly, α-tocopherol does not modulate cell migration and capillary-like tube formation although at the concentration of 20 and 40 μmol/L it potentiated PMA-induced DNA synthesis (P < 0.05).Our results suggest that although α-tocopherol supplementation reduces endothelial cell oxidative stress, it does not alter the cell response to angiogenic stimuli.