Platelet binding and phagocytosis by macrophages.
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.


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.


CONCLUSIONS
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.
Badlou
Bahram A
BA
Thrombosis and Hemostasis Laboratory, Department of Hematology, University Medical Center Utrecht, the Netherlands.
Wu
Ya Ping
YP
Smid
W Martin
WM
Akkerman
Jan-Willem N
JW
D001793:Blood Preservation / Q000009:adverse effects; D002460:Cell Line; D002470:Cell Survival; D006801:Humans; D008264:Macrophages / Q000378:metabolism; D019007:P-Selectin / Q000378:metabolism; D010587:Phagocytosis; D010973:Platelet Adhesiveness; D017713:Platelet Transfusion
D019007:P-Selectin