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Inhibition of platelet-derived mitogen release by nitric oxide (EDRF)
M L Barrett1, A L Willis, J R Vane
1William Harvey Research Institute, St. Bartholomew's Hospital Medical College, London, UK.
Agents and Actions
|June 1, 1989
Summary
Nitric oxide (NO) inhibits the release of mitogens from activated human platelets, a process crucial for cell growth. This finding suggests NO
Area of Science:
- Biochemistry
- Cell Biology
- Physiology
Background:
- Platelets aggregate and release mitogenic substances upon exposure to thrombogenic surfaces.
- Endothelium-derived relaxing factor (EDRF), identified as nitric oxide (NO), is known to inhibit platelet aggregation.
Purpose of the Study:
- To investigate the effect of nitric oxide (NO) on mitogen release from stimulated human platelets.
- To determine if NO can inhibit the mitogenic activity released from aggregated platelets.
Main Methods:
- Mitogenic activity was assessed using 3H-thymidine incorporation in mouse fibroblast 3T3 cells.
- Human platelets were stimulated with collagen, and the resulting serum was tested for mitogenic effects.
- The impact of NO and prostacyclin on platelet aggregation and mitogen release was evaluated in a dose-dependent manner.
Main Results:
- Serum from collagen-aggregated platelets significantly increased 3H-thymidine incorporation in 3T3 cells compared to control.
- Both platelet aggregation and the increase in mitogenic activity were inhibited by NO and prostacyclin in a dose-related manner.
- The inhibitory effect of NO on mitogen release decayed over time in platelet-free plasma but remained detectable for at least 2 minutes.
Conclusions:
- Nitric oxide (NO) effectively inhibits mitogen release from stimulated human platelets.
- NO and prostacyclin share inhibitory effects on both platelet aggregation and mitogen release.
- NO's inhibitory action on mitogen release is relatively stable in plasma, suggesting potential physiological relevance.