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Updated: Jul 5, 2026
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A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
Published on: June 5, 2019
Expression of complement components and inhibitors on platelet microparticles.
Wei Yin1, Berhane Ghebrehiwet, Ellinor I B Peerschke
1Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, NY, USA.
Platelets
|April 25, 2008
Summary
Platelet microparticles (PMP) can activate the complement system, a key part of immune response. This finding links PMP to inflammatory and vascular diseases like atherosclerosis.
Area of Science:
- Immunology
- Hematology
- Biochemistry
Background:
- Platelet microparticles (PMP) originate from activated platelets and are implicated in hemostasis, thrombosis, and inflammation.
- Platelets possess intrinsic capabilities for activating both classical and alternative complement pathways.
Purpose of the Study:
- To investigate the capacity of PMP to activate the complement system.
- To determine the role of PMP in complement-mediated inflammatory processes.
Main Methods:
- PMP generation via platelet activation with A23187.
- PMP identification using flow cytometry (size, Annexin V, P-selectin, CD41).
- Analysis of complement regulatory proteins (gC1qR/p33, C1-INH, CD55, CD59) and complement activation markers (C4, C3b, C5b-9) on PMP.
Main Results:
- PMP express gC1qR/p33, C1-INH, CD55, and CD59.
- PMP support classical complement pathway activation (C4) despite C1-INH presence.
- Significant deposition of C3b and C5b-9 occurs on PMP when exposed to plasma.
Conclusions:
- This study provides the first evidence that PMP can support complement activation in situ.
- PMP-mediated complement activation may contribute to vascular and inflammatory diseases such as atherosclerosis and ischemia/reperfusion injury.
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