Platelet Adhesion Analysis
Platelet Adhesion Analysis - Related Videos
10:10
Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
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Cited by 29 •
2009
The platelet adhesion cascade takes place in the presence of shear flow, a factor not accounted for in conventional (static) well-plate assays. This article reports on a platelet-aggregation assay utilizing a microfluidic well-plate format to emulate physiological shear flow conditions.
06:04
LC-MS Analysis of Human Platelets as a Platform for Studying Mitochondrial Metabolism
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Cited by 7 •
2016
Here we show isolated human platelets can be used as an accessible ex vivo model to study metabolic adaptations in response to the complex I inhibitor rotenone. This approach employs isotopic tracing and relative quantification by liquid chromatography-mass spectrometry and can be applied to a variety of study designs.
10:08
Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets
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Cited by 2 •
2024
This article outlines the protocol for quantifying the percentage of Tissue Factor (TF)-positive platelets using whole blood flow cytometry, assessing the protein: (1) intracellularly in resting conditions, and (2) on the cell surface, in both resting and activated conditions. Guidance is also provided for evaluating TF-positive platelets in platelet-rich plasma.
09:38
A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
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Cited by 13 •
2017
This paper describes an experimental model of hemostasis that simultaneously measures platelet function and coagulation. Platelet and fibrin fluorescence is measured in real-time, and platelet adhesion rate, coagulation rate, and onset of coagulation are determined. The model is used to determine platelet procoagulant properties under flow in concentrates for transfusion.
05:42
A Turbidimetric Analysis to Monitor Collagen-Induced Aggregation of Pretreated Human Platelets
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2025
This video demonstrates turbidimetric analysis to assess collagen-induced platelet aggregation in pre-treated, washed human platelets. Control wells show collagen-induced aggregation, whereas a high concentration of inhibitors blocks Pannexin-1 channels, thereby inhibiting collagen-induced platelet aggregation, evident from unchanged turbidity.
FAQs
Blood flow helps distinguish transient platelet tethering from firm adhesion. Under these conditions, platelet receptors first engage exposed extracellular matrix proteins, particularly von Willebrand factor and collagen, allowing circulating cells to slow and attach. Subsequent receptor interactions and platelet activation strengthen retention, making flow-dependent assays useful for resolving early adhesive events.
Von Willebrand factor and collagen provide distinct extracellular binding surfaces exposed after vascular damage or cellular activation. Platelet receptors recognize these proteins and support sequential attachment under flow, linking the initial contact of circulating platelets to more stable adhesion. Measuring responses to these coated components can reveal how receptor-mediated interactions change during inflammation or infection.
Adhesion is not only a physical attachment event; it can be followed by platelet activation, which changes how strongly platelets remain associated with a surface and how they communicate with neighboring cells. Consequently, an adhesion assay can provide insight into the transition from initial binding to a more biologically active state relevant to vascular inflammation and thrombosis.
Comparing platelet attachment under controlled conditions with samples exposed to inflammatory signals or infectious agents can show whether those stimuli alter interactions with extracellular matrix proteins or vascular cells. Changes in adhesion help characterize infection-associated thromboinflammation and may indicate altered communication among platelets, endothelial cells, immune components, and pathogens.
Common assay formats examine platelet attachment to surfaces coated with relevant extracellular matrix proteins or to vascular cells. Protein-coated surfaces focus attention on defined adhesive interactions, whereas vascular-cell models provide context for platelet communication with the endothelium. Using either format can help connect receptor binding with broader vascular responses.
The analysis can characterize how platelets participate in host defense, vascular injury, and infection-associated thromboinflammation. Results may clarify whether infectious agents or inflammatory conditions modify platelet interactions with endothelial cells, immune components, or pathogens. This makes adhesion measurements useful for linking cellular binding behavior to immunological and vascular consequences of infection.