Endothelial progenitor cells inhibit platelet function in a P-selectin-dependent manner
Haissam Abou-Saleh1, Ahmed Hachem2, Daniel Yacoub3
1Qatar Cardiovascular Research Center, Qatar Foundation, Education City, Doha, Qatar. hasaleh@qf.org.qa.
Journal of Translational Medicine
|May 8, 2015
Summary
Endothelial progenitor cells (EPCs) reduce blood clot formation by binding to platelet P-selectin. This interaction is crucial for EPCs
Area of Science:
- Cardiovascular Biology
- Hematology
- Cell Biology
Background:
- Endothelial progenitor cells (EPCs) play a role in vascular repair by interacting with circulatory components.
- Previous studies indicated EPCs inhibit platelet function and thrombus formation, but the role of P-selectin binding was unclear.
Purpose of the Study:
- To assess the impact of EPCs on thrombus formation.
- To investigate the implication of platelet P-selectin in EPC-mediated regulation of thrombosis.
Main Methods:
- EPCs were generated from human peripheral blood mononuclear cells.
- The effects of EPCs on platelet aggregation and thrombus formation were studied in P-selectin deficient (P-sel(-/-)) and wild-type (WT) mice.
Main Results:
- EPCs impaired collagen-induced platelet aggregation in WT mice but not in P-sel(-/-) mice.
- EPC infusion reduced thrombus formation in WT mice, but not in P-sel(-/-) mice.
- Thrombi were larger and EPC recruitment was reduced in P-sel(-/-) mice compared to WT mice.
Conclusions:
- EPCs reduce platelet aggregation and thrombus formation through a mechanism involving binding to platelet P-selectin.
- This highlights the significance of EPC-platelet interactions in regulating thrombotic events during vascular repair.
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