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Nitric oxide induces and inhibits apoptosis through different pathways
Y H Shen1, X L Wang, D E Wilcken
1Department of Cardiovascular Medicine, University of New South Wales, Prince of Wales Hospital, Randwick, Australia.
FEBS Letters
|September 17, 1998
Summary
Low nitric oxide (NO) levels protect human endothelial cells, while high NO concentrations trigger cell death. The study reveals NO
Area of Science:
- Biomedical Science
- Cell Biology
- Physiology
Background:
- Nitric oxide (NO) plays a crucial role in regulating vascular tone and protecting microvasculature.
- Dysregulation of NO levels can lead to harmful effects, including endothelial cell injury.
Purpose of the Study:
- To investigate the dual effects of nitric oxide (NO) on human endothelial cell apoptosis.
- To elucidate the role of the cyclic guanosine monophosphate (cGMP) pathway in NO-mediated endothelial cell survival and apoptosis.
Main Methods:
- Utilized the NO donor S-nitroso-N-acetylpenicillamine (SNAP) to modulate NO levels in human endothelial cells.
- Assessed endothelial cell apoptosis in response to varying SNAP concentrations and investigated the involvement of the cGMP pathway.
Main Results:
- Low concentrations of SNAP (NO donor) inhibited tumor necrosis factor-alpha (TNFα)-induced endothelial apoptosis, partly via the cGMP pathway.
- High concentrations of SNAP induced endothelial cell apoptosis through cGMP-independent mechanisms.
- The cGMP pathway demonstrated a protective role against NO-induced apoptosis.
Conclusions:
- Physiological levels of NO promote human endothelial cell survival.
- Pathological concentrations of NO are detrimental, inducing endothelial cell apoptosis via cGMP-independent pathways.
- NO exhibits a dose-dependent, biphasic effect on endothelial cell fate, highlighting its complex role in vascular health.