Key Points
- To examine the concentration-dependent mechanisms through which nitric oxide promotes or inhibits apoptosis in human endothelial cells.
- Treated cultured human endothelial cells with varying concentrations of the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP).
- Evaluated endothelial apoptosis following tumor necrosis factor-alpha exposure with and without cGMP pathway modulation.
- Low concentrations of the nitric oxide donor SNAP inhibited tumor necrosis factor-alpha-induced endothelial apoptosis, an effect partially mediated by the cGMP pathway.
- High concentrations of SNAP triggered endothelial cell apoptosis through cGMP-independent pathways, whereas activation of the cGMP pathway conferred protection against nitric oxide-induced cell death.
Structured PICO
PPopulationHuman endothelial cells
IInterventionNO donor S-nitroso-N-acetylpenicillamine (SNAP) at varying concentrations
OOutcomeEndothelial cell apoptosissurrogate
Nitric oxide exerts a biphasic effect on human endothelial cells, promoting survival at low concentrations and inducing apoptosis at high concentrations.