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Ultrastructural changes in endothelium during apoptosis indicate low microembolic potential.
Wei Xu1, Ross Boadle, Levina Dear
1Cellular and Molecular Pathology Research Unit, Department of Oral Pathology and Oral Medicine, University of Sydney, Westmead Centre for Oral Health S, Westmead, Australia.
Journal of Vascular Research
|August 10, 2005
Summary
Endothelial apoptosis reduces cell size and increases circularity, aiding passage through vessels. Canalicular fragmentation is key to minimizing microembolic potential from apoptotic endothelial cells.
Area of Science:
- Cell Biology
- Vascular Biology
- Pathology
Background:
- Apoptotic endothelium may cause microthrombosis and microemboli.
- Conflicting reports exist on its pro-coagulant and fibrinolytic activities.
- Endothelial canalicular fragmentation is unique and may reduce microemboli size.
Purpose of the Study:
- Characterize cell size and shape changes during endothelial apoptosis.
- Investigate the role of canalicular fragmentation in mitigating microembolic risk.
Main Methods:
- Transmission and scanning electron microscopy of apoptotic endothelium.
- Comparison with apoptotic HL-60 cells lacking canalicular fragmentation.
Main Results:
- Apoptotic endothelium showed reduced size compared to HL-60 cells.
- Mechanical stress accelerated size reduction and increased circularity in apoptotic endothelium.
- Canaliculi formation involves vesicle fusion, leading to vacuoles and dilation in late apoptosis.
Conclusions:
- Endothelium exhibits adaptations to minimize microembolic potential.
- Canalicular fragmentation plays a significant role in reducing the microembolic risk of apoptotic endothelial cells.