Nitric oxide induces and inhibits apoptosis through different pathways

FEBS Letters

Wang, Xing L¹  Shen, Ying H¹  Wilcken, David E.L¹ 

[1] Department of Cardiovascular Medicine, University of New South Wales, Prince of Wales Hospital, Ground Floor, South Wing, Edmund Blacket Building, Randwick, NSW 2031, Australia

关键词: Nitric oxide;    Tumor necrosis factor α;    Apoptosis;    Endothelial cell;    cGMP;    Atherosclerosis;    NO;    nitric oxide;    TNFα;    tumour necrosis factor alpha;    SNAP;    S-nitroso-N-acetylpenicillamine;    NOS;    nitric oxide synthase;    HUVEC;    human venous endothelial cells;    ECGF;    endothelial cell growth factor;    ODQ;    guanylyl cyclase inhibitor 1H-[1;    2;    4]oxadiazolo[4;    3-a]quinoxalin-1-one;    LDH;    lactate dehydrogenase;   

DOI  :  10.1016/S0014-5793(98)00844-8

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown