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Ambient pulsatile pressure modulates endothelial cell proliferation
A G Vouyouka1, R J Powell, J Ricotta
1Departments of Surgery, Yale University School of Medicine, New Haven, CT, USA.
Journal of Molecular and Cellular Cardiology
|May 9, 1998
Summary
Pulsatile pressure significantly inhibits endothelial cell proliferation by day 5. This effect is mediated by an autocrine factor secreted by cells exposed to pulsatile pressure, not TGF-beta or IL-1.
Area of Science:
- Cardiovascular Biology
- Cell Biology
- Biomedical Engineering
Background:
- Circulatory forces like shear stress and strain impact endothelial cell (EC) phenotype.
- The in vitro effects of direct pressure on EC remain largely unexplored.
Purpose of the Study:
- To investigate the in vitro effects of static and pulsatile pressure on cultured endothelial cells.
- To elucidate the mechanism behind pressure-induced changes in EC proliferation.
Main Methods:
- Cultured bovine aortic EC were exposed to atmospheric, static (135 mmHg), or pulsatile (160/110 mmHg, 60 cycles/min) pressure.
- EC proliferation was assessed via cell counting and 3H-thymidine incorporation.
- Conditioned media transfer experiments were performed to investigate autocrine signaling.
Main Results:
- A significant decrease in EC cell number was observed by day 5 in both static and pulsatile pressure groups.
- Cell morphology and viability remained unchanged across all conditions.
- Conditioned media from pulsatile pressure-exposed EC inhibited proliferation in control EC, suggesting an autocrine factor.
Conclusions:
- Pulsatile pressure induces an autocrine growth inhibitory effect in endothelial cells.
- This inhibitory effect is not mediated by TGF-beta or IL-1.
- Endothelial cells secrete autocrine factors in response to pulsatile pressure, influencing their proliferation.