Publisher： Spandidos Publications
ISSN： 1107-3756
Source： International Journal of Molecular Medicine, Vol.31, Iss.2, 2013-01, pp. : 471-476
Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.
Abstract
Enhanced oxidative stress contributes to endothelial dysfunction via the apoptotic induction of endothelial cells (ECs). However, the precise molecular mechanisms underlying its important effect remain unclear. Here, we evaluated the effects of exogenous hydrogen peroxide (H2O2) on cell growth and death in ECs such as calf pulmonary artery endothelial cells (CPAECs) and human umbilical vein endothelial cells (HUVECs) and investigated its mechanism of action in CPAECs. H2O2 inhibited the growth of CPAECs and HUVECs at 24 h with IC50 of approximately 20 and 300 µM, respectively. H2O2 induced cell death in both ECs, which was accompanied by the loss of mitochondrial membrane potential (MMP; ∆Ψm). H2O2-induced CPAEC death occurred via apoptosis, demonstrated by Annexin V-staining cells and Z-VAD (a pan-caspase inhibitor) treatment. H2O2 increased superoxide anion levels in HUVECs but not in CPAECs. Treatment with 30 µM H2O2 significantly decreased the activities of superoxide dismutases and catalase in CPAECs. H2O2 induced glutathione (GSH) depletion in both ECs. Z-VAD and N-acetyl cysteine (NAC; a well-known antioxidant) attenuated apoptotic cell death and GSH depletion in H2O2-treated CPAECs. In conclusion, H2O2 induced growth inhibition and death in ECs via GSH depletion. HUVECs were relatively resistant to H2O2 compared with CPAECs. H2O2-induced CPAEC apoptosis required the activation of various caspases.
Related content
Access to resources
Recommend
CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY (ELECTRONIC), Vol. 42, Iss. 6, 2015-06 ,pp. :