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The effect of hydroxychloroquine on platelet activation in model experiments
Karen Schreiber1,2,3, Savino Sciascia4, Florian Wehrmann5
1Danish Hospital for Rheumatic Diseases, Sønderborg, Denmark.
Journal of Thrombosis and Thrombolysis
|January 2, 2021
Summary
Hydroxychloroquine (HCQ) may reduce platelet activation, particularly in the presence of specific endothelial cells. Direct HCQ exposure to platelets, however, increases activation markers, suggesting an endothelial-mediated effect.
Area of Science:
- Immunology
- Hematology
- Pharmacology
Background:
- Hydroxychloroquine (HCQ) is a key treatment for autoimmune diseases.
- Clinical observations suggest HCQ possesses anti-thrombotic properties.
- The precise mechanism of HCQ's anti-thrombotic effect requires elucidation.
Purpose of the Study:
- To investigate the effect of HCQ on platelet activation.
- To determine the role of endothelial cells in HCQ's impact on platelet activation.
- To explore the expression of CD40L as a marker of platelet activation.
Main Methods:
- Human umbilical vein endothelial cells (HUVECs) and human umbilical arterial endothelial cells (HUAECs) were incubated with HCQ.
- Cells were stimulated with tumor necrosis factor alpha (TNF-α) and thrombin-activated platelets.
- Platelet activation was assessed by measuring CD40L expression via flow cytometry.
Main Results:
- Direct incubation of platelets with HCQ increased CD40L expression.
- Pre-incubation of HUAECs with HCQ significantly reduced CD40L expression on platelets after stimulation.
- HCQ pre-incubation of HUVECs did not significantly reduce CD40L expression.
- HCQ reduced the stimulatory effect of TNF-α and thrombin on platelet activation in the presence of HUAECs.
Conclusions:
- HCQ exhibits an endothelial-mediated reduction in platelet activation, specifically involving HUAECs.
- The anti-thrombotic effects of HCQ may be linked to its interaction with endothelial cells.
- Further research is warranted to fully understand HCQ's complex effects on platelet function.
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