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Updated: Jun 7, 2026
Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
Published on: October 27, 2009
Internalization of microparticles by endothelial cells promotes platelet/endothelial cell interaction under flow
A D Terrisse1, N Puech, S Allart
1INSERM (Institut National de la Santé Et de la Recherche Médicale), U858- I2MR, Toulouse, France. aterriss@cict.fr
Background:
Microparticles (MPs) released by activated or apoptotic cells increase in number in the blood of subjects with vascular or metabolic diseases and may contribute to thrombotic complications.
Objectives:
In this study, we investigated whether MPs promoted platelet recruitment to endothelial cells in flow conditions, and by which mechanism.
Methods:
Human umbilical vein endothelial cells (HUVECs) grown in microslide perfusion chambers were exposed to MPs prepared in vitro from HUVECs, monocytes or platelets.
Results:
Videomicroscopy of DIOC-labelled blood perfused at arterial rate on human umbilical vein ECs demonstrated that, irrespective of their cell origin, MPs promoted the formation of platelet strings at the surface of HUVECs. This platelet/endothelial cell interaction was dependent on von Willebrand factor (VWF) expression at the HUVEC surface and involved Glycoprotein Ib and P-selectin. Interestingly, HUVECs internalized MPs within a few hours through a process involving anionic phospholipids, lactadherin and αvβ3 integrin. This uptake generated the production of reactive oxygen species via the xanthine/xanthine oxidase system (inhibited by allopurinol and the ROCK inhibitor Y-27632) and the NADPH oxidase (inhibited by SOD). Reactive oxygen species appeared essential for VWF expression at the endothelial cell surface and subsequent platelet/endothelial cell interaction under flow. The pathophysiological relevance of this process is underlined by the fact that circulating MPs from Type I diabetic patients induced platelet/endothelial cell interaction under flow, with an intensity correlated with the severity of the vasculopathy.
Insights
Microparticles (MPs) from various cells promote platelet adhesion to endothelial cells via von Willebrand factor. This interaction, crucial in vascular diseases, is mediated by reactive oxygen species generated during MP uptake.
Area of Science:
- Cardiovascular Biology
- Cellular Biology
- Thrombosis Research
Background:
- Microparticles (MPs) increase in vascular and metabolic diseases, potentially causing thrombotic complications.
- MPs are released from activated or apoptotic cells.
Purpose of the Study:
- To investigate if MPs promote platelet recruitment to endothelial cells under flow conditions.
- To elucidate the underlying mechanisms of MP-induced platelet recruitment.
Main Methods:
- Human umbilical vein endothelial cells (HUVECs) were exposed to MPs in microslide perfusion chambers.
- Videomicroscopy and specific inhibitors were used to analyze interactions and pathways.
Main Results:
- MPs, regardless of origin, induced platelet string formation on HUVECs, dependent on VWF, Glycoprotein Ib, and P-selectin.
- HUVECs internalized MPs via anionic phospholipids, lactadherin, and αvβ3 integrin, generating reactive oxygen species (ROS).
- ROS production was essential for VWF expression and subsequent platelet-endothelial cell interaction; patient MPs from Type I diabetics showed correlated interaction intensity with vasculopathy severity.
Conclusions:
- MPs promote platelet recruitment to endothelial cells through a ROS-dependent mechanism involving VWF.
- This process contributes to thrombotic complications in vascular diseases, as evidenced by diabetic patient data.
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