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Nitric oxide induces and inhibits apoptosis through different pathways
Author(s) -
Shen Ying H,
Wang Xing L,
Wilcken David E.L
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)00844-8
Subject(s) - apoptosis , nitric oxide , snap , microbiology and biotechnology , endothelial stem cell , chemistry , signal transduction , downregulation and upregulation , cell , biology , biochemistry , endocrinology , in vitro , computer graphics (images) , computer science , gene
Physiological levels of nitric oxide (NO) regulate vascular tone and protect the microvasculature from injury whereas excessive NO may be harmful. The present study explored the effects of NO on human endothelial cell apoptosis. We found that the NO donor S ‐nitroso‐ N ‐acetylpenicillamine (SNAP) inhibited TNFα‐induced endothelial apoptosis and that this was mediated partly through the cGMP pathway. In contrast, high SNAP concentration induced endothelial apoptosis via cGMP‐independent pathways and the cGMP pathway protected against NO‐induced apoptosis. These findings demonstrate that low NO concentrations contribute to human endothelial cell survival, whereas higher NO concentrations are pathological and promote destruction of endothelial cells.