Oxidative stress and angiogenesis are important elements in the pathogenesis of atherosclerosis and cancer. Because of its antioxidant properties, alpha-tocopherol has long proposed as prevention of diseases associated with oxidative stress. We explore whether alpha-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 alpha-tocopherol treatment (540 µmol/L) for 72 h on the production of reactive oxygen species (ROS), induction of matrix metalloproteinases (MMPs), expression of vascular endothelialcadherin (VE-cadherin) and alpha2 -integrin, cell migration, cell proliferation, and tube formation. alpha-Tocopherol significantly inhibits intracellular ROS production induced by TNF-alpha (P 0.01) or PMA (P 0.001). However, alpha-tocopherol does not interfere with mRNA expression of VE-cadherin, alpha2 -integrin, MMP-1, MMP-2, and MMP-9. Similarly, alpha-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 alpha-tocopherol supplementation reduces endothelial cell oxidative stress, it does not alter the cell response to angiogenic stimuli.
Lack of effect of alpha-tocopherol on in vitro angiogenesis
Battaglia D;
2006
Abstract
Oxidative stress and angiogenesis are important elements in the pathogenesis of atherosclerosis and cancer. Because of its antioxidant properties, alpha-tocopherol has long proposed as prevention of diseases associated with oxidative stress. We explore whether alpha-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 alpha-tocopherol treatment (540 µmol/L) for 72 h on the production of reactive oxygen species (ROS), induction of matrix metalloproteinases (MMPs), expression of vascular endothelialcadherin (VE-cadherin) and alpha2 -integrin, cell migration, cell proliferation, and tube formation. alpha-Tocopherol significantly inhibits intracellular ROS production induced by TNF-alpha (P 0.01) or PMA (P 0.001). However, alpha-tocopherol does not interfere with mRNA expression of VE-cadherin, alpha2 -integrin, MMP-1, MMP-2, and MMP-9. Similarly, alpha-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 alpha-tocopherol supplementation reduces endothelial cell oxidative stress, it does not alter the cell response to angiogenic stimuli.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
