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Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
Published on: October 27, 2009
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Circulating platelet aggregates damage endothelial cells in culture.
Chandrakala Aluganti Narasimhulu1, Mukesh Nandave2, Diana Bonilla3
1Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida.
The Journal of Surgical Research
|June 12, 2017
Summary
Aggregated platelets (AgPlts) disrupt the endothelium, causing the release of circulating endothelial cells (CECs) and endothelial-derived particles (ECDPs). This mechanical disruption by AgPlts is a key mechanism of endothelial damage.
Area of Science:
- Cardiovascular Biology
- Endothelial Function
- Platelet Biology
Background:
- Circulating endothelial cells (CECs) and endothelial-derived particles (ECDPs) may indicate endothelial damage and repair processes.
- Aggregated platelets (AgPlts) are hypothesized to contribute to endothelial disruption and the release of CECs and ECDPs.
Purpose of the Study:
- To investigate the effect of aggregated platelets (AgPlts) on endothelial integrity.
- To determine if AgPlts can cause endothelial denudation and release CECs and ECDPs.
Main Methods:
- Endothelial cells (ECs) in a flow system were exposed to medium, nonaggregated platelets (NAgPlts), AgPlts, or polystyrene beads.
- Effluents were analyzed for CECs and ECDPs, and endothelial damage was assessed via RT-PCR and Western blot for von Willebrand factor.
Main Results:
- AgPlts and polystyrene beads significantly dislodged ECs, releasing CECs and ECDPs into the effluent.
- Endothelial damage markers, including von Willebrand factor, were elevated in effluents from damaged endothelium.
- CECs and ECDPs were also detected in plasma samples from heart failure subjects and animals.
Conclusions:
- Circulating aggregated platelets (AgPlts) actively denude the endothelium, leading to the release of CECs and ECDPs.
- Mechanical disruption and shear stress from AgPlts are likely mechanisms driving endothelial damage.
- These findings highlight a novel pathway for endothelial injury involving platelet aggregation.
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