期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2003
卷号：100
期号：19
页码：10653-10658
DOI：10.1073/pnas.1933581100
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：We investigated here the mechanism of cytoprotection of nitric oxide ([bullet]NO) in bovine aortic endothelial cells treated with H2O2. NONOates were used as [bullet]NO donors that released [bullet]NO slowly at a well defined rate in the extracellular and intracellular milieus. H2O2-mediated intracellular dichlorofluorescein fluorescence and apoptosis were enhanced by the transferrin receptor (TfR)-mediated iron uptake. [bullet]NO inhibited the TfR-mediated iron uptake, dichlorofluorescein fluorescence, and apoptosis in H2O2-treated cells. [bullet]NO increased the proteasomal activity and degradation of nitrated TfR via ubiquitination. N{omega}-nitro-L-arginine methyl ester, a nonspecific inhibitor of endogenous [bullet]NO biosynthesis, decreased the trypsin-like activity of 26S proteasome. [bullet]NO, by activating proteolysis, mitigates TfR-dependent iron uptake, dichlorodihydrofluorescein oxidation, and apoptosis in H2O2-treated bovine aortic endothelial cells. The relevance of biological nitration on redox signaling is discussed.
