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Updated: Feb 20, 2026

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets
Published on: April 9, 2018
Molecular and functional interactions among monocytes, platelets, and endothelial cells and their relevance for
Janine M van Gils1, Jaap Jan Zwaginga, Peter L Hordijk
1Department of Molecular Cell Biology, Sanquin Research and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Insights
Platelets and monocytes drive cardiovascular disease by promoting inflammation. Their interactions with endothelial cells involve adhesion molecules and chemokines, crucial for disease progression.
Area of Science:
- Cardiovascular Biology
- Immunology
- Cellular Biology
Background:
- Cardiovascular diseases (CVDs) are significantly influenced by inflammation.
- Platelets, monocytes, and endothelial cells play critical roles in CVD development and progression.
- Inflammation in CVDs is amplified by platelet activation and adhesion to the endothelium.
Purpose of the Study:
- To review the complex interactions between platelets, monocytes, and endothelial cells.
- To elucidate the functional implications of these interactions in inflammation and CVD.
- To highlight the molecular mechanisms governing cell-cell interactions in CVD.
Main Methods:
- Review of scientific literature on platelet-endothelial-monocyte interactions.
- Analysis of molecular mechanisms involving chemokines and adhesion molecules.
- Examination of the roles of selectins, integrins, and their ligands.
Main Results:
- Activated platelets and platelet-monocyte complexes mediate inflammation and leukocyte recruitment.
- Endothelial cells express adhesion molecules (selectins, integrins) and chemokines that regulate cell interactions.
- Platelet-derived chemokines and endothelial adhesion molecules promote monocyte recruitment and migration.
Conclusions:
- Platelets are key mediators of inflammation in cardiovascular disorders.
- Complex molecular interactions between platelets, monocytes, and endothelium drive CVD.
- Understanding these interactions is vital for developing therapeutic strategies against CVD.
Abstract:
Platelets, monocytes, and endothelial cells are instrumental in the development and progression of cardiovascular diseases. Inflammation, a key process underlying cardiovascular disorders, is accompanied and amplified by activation of platelets and consequent binding of such platelets to the endothelium. There, platelet-derived chemokines, in conjunction with increased expression of adhesion molecules, promote the recruitment of circulating monocytes that will eventually migrate across the endothelial lining of the vessel into the tissues. Additionally, platelets may already become activated in the circulation and may form platelet-monocyte complexes, which show increased adhesive and migratory capacities themselves but also facilitate recruitment of noncomplexed leukocytes. They should therefore be considered as important mediators of inflammation. In molecular terms, these events are additionally governed by chemokines released and presented by the endothelium as well as the different classes of endothelial adhesion molecules that regulate the interactions among the various cell types. Most important in this respect are the selectins and their ligands, such as P-selectin glycoprotein (GP) ligand 1, and the integrins binding to Ig-like cell adhesion molecules as well as to GP, such as von Willebrand factor, present in the extracellular matrix or on activated endothelium. This review aims to provide an overview of these complex interactions and of their functional implications for inflammation and development of cardiovascular disease.
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