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Platelet binding and phagocytosis by macrophages
Author(s) -
Badlou Bahram A.,
Wu Ya Ping,
Smid W. Martin,
Akkerman JanWillem N.
Publication year - 2006
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1111/j.1537-2995.2006.00913.x
Subject(s) - phagocytosis , platelet , phosphatidylserine , chemistry , flow cytometry , phagosome , microbiology and biotechnology , immunology , biology , biochemistry , phospholipid , membrane
BACKGROUND: Earlier it was reported that metabolic arrest followed by incubation at 4°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) Ibα clustering. It was found that trapping of PLT Ca 2+ and raising cAMP reduces phagocytosis by lowering PS exposure. Chilling of PLTs leads to an increase in binding and PS‐ and GPIbα‐mediated phagocytosis. Prior depletion of PLT energy stores prevents this increase by preserving low Ca 2+ 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.