一氧化氮抑制过氧化氢诱导的内皮细胞中依赖转铁蛋白受体的细胞凋亡：泛素-蛋白酶体途径的作用
Nitric oxide inhibits H2O2-induced transferrin receptor-dependent apoptosis in endothelial cells: Role of ubiquitin-proteasome pathway.
作者信息
Kotamraju Srigiridhar, Tampo Yoshiko, Keszler Agnes, Chitambar Christopher R, Joseph Joy, Haas Arthur L, Kalyanaraman B
机构信息
Biophysics Research Institute and Free Radical Research Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
出版信息
Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):10653-8. doi: 10.1073/pnas.1933581100. Epub 2003 Sep 4.
Abstract
We investigated here the mechanism of cytoprotection of nitric oxide (*NO) in bovine aortic endothelial cells treated with H2O2. NONOates were used as *NO donors that released *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. *NO inhibited the TfR-mediated iron uptake, dichlorofluorescein fluorescence, and apoptosis in H2O2-treated cells. *NO increased the proteasomal activity and degradation of nitrated TfR via ubiquitination. Nomega-nitro-L-arginine methyl ester, a nonspecific inhibitor of endogenous *NO biosynthesis, decreased the trypsin-like activity of 26S proteasome. *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.
摘要
我们在此研究了一氧化氮（NO）对经过氧化氢（H2O2）处理的牛主动脉内皮细胞的细胞保护机制。NONOate被用作NO供体，其在细胞外和细胞内环境中以明确的速率缓慢释放*NO。转铁蛋白受体（TfR）介导的铁摄取增强了H2O2介导的细胞内二氯荧光素荧光和细胞凋亡。*NO抑制了H2O2处理细胞中TfR介导的铁摄取、二氯荧光素荧光和细胞凋亡。NO通过泛素化增加了蛋白酶体活性以及硝化TfR的降解。Nω-硝基-L-精氨酸甲酯，一种内源性NO生物合成的非特异性抑制剂，降低了26S蛋白酶体的胰蛋白酶样活性。*NO通过激活蛋白水解作用，减轻了H2O2处理的牛主动脉内皮细胞中TfR依赖性铁摄取、二氯二氢荧光素氧化和细胞凋亡。本文讨论了生物硝化作用对氧化还原信号传导的相关性。
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