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Updated: Feb 28, 2026
Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
Published on: October 27, 2009
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.
Insights
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.
Background:
Presence of circulating endothelial cells (CECs) in systemic circulation may be an indicator of endothelial damage and/or denudation, and the body's response to repair and revascularization. Thus, we hypothesized that aggregated platelets (AgPlts) can disrupt/denude the endothelium and contribute to the presence of CEC and EC-derived particles (ECDP).
Methods:
Endothelial cells were grown in glass tubes and tagged with/without 0.5 μm fluorescent beads. These glass tubes were connected to a mini-pump variable-flow system to study the effect of circulating AgPlts on the endothelium. ECs in glass tube were exposed to medium alone, nonaggregated platelets (NAgPlts), AgPlts, and 90 micron polystyrene beads at a flow rate of 20 mL/min for various intervals. Collected effluents were cultured for 72 h to analyze the growth potential of dislodged but intact ECs. Endothelial damage was assessed by real time polymerase chain reaction (RT-PCR) for inflammatory genes and Western blot analysis for von Willebrand factor.
Results And Conclusion:
No ECs and ECDP were observed in effluents collected after injecting medium alone and NAgPlts, whereas AgPlts and Polybeads drastically dislodged ECs, releasing ECs and ECDP in effluents as the time increased. Effluents collected when endothelial cell damage was seen showed increased presence of von Willebrand factor as compared to control effluents. Furthermore, we analyzed the presence of ECs and ECDPs in heart failure subjects, as well as animal plasma samples. Our study demonstrates that circulating AgPlts denude the endothelium and release ECs and ECDP. Direct mechanical disruption and shear stress caused by circulating AgPlts could be the underlying mechanism of the observed endothelium damage.
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