BACKGROUND: Earlier it was reported that metabolic arrest followed by incubation at 4 degrees C reduces the platelet (PLT) storage defect. Here it is reported that this treatment also reduces binding and phagocytosis by macrophages.
STUDY DESIGN AND METHODS: Phagocytosis of mepacrine-labeled PLTs by macrophages changes the latter into bright fluorescent particles easily detected by fluorescence-activated cell sorting.
RESULTS: In combination with conventional binding analysis it was found that binding to phorbol 12-myristate 13-acetate-matured THP-1 cells is primarily regulated by PLT P-selectin expression and phagocytosis by combined phosphatidylserine (PS) exposure and glycoprotein (GP) Ibalpha clustering. It was found that trapping of PLT Ca2+ and raising cAMP reduces phagocytosis by lowering PS exposure. Chilling of PLTs leads to an increase in binding and PS- and GPIbalpha-mediated phagocytosis. Prior depletion of PLT energy stores prevents this increase by preserving low Ca2+ concentration, PS exposure, and PS-mediated phagocytosis.
CONCLUSION: These data characterize the individual factors that control PLT binding and phagocytosis and might help to define conditions that improve the survival of stored PLTs after transfusion.
- Blood Preservation/adverse effects
- Cell Line
- Cell Survival
- Platelet Adhesiveness
- Platelet Transfusion