oxLDL stimulates tyrosine phosphorylation of the FcRγ. (A) Washed human platelets (7 × 10⁸/mL) were either untreated or treated with oxLDL (50 μg/mL) or nLDL (50 μg/mL) for 15 seconds. FcRγ was immunoprecipitated from lysates and immunoblotted for phospho-tyrosine and FcRγ; representative blots (upper) and densitometric analysis (lower) of 5 independent experiments. ∗P < .05. (B) As in panel A, except platelets were stimulated with increasing concentrations of oxLDL (10-100 μg/mL). Representative blots (upper) and densitometric analysis (lower) of 5 independent experiments. ∗P < .05. (C) As in panel A, except platelets were stimulated with oxLDL (50 μg/mL) for up to 300 seconds. Representative blots (upper) and densitometric analysis (lower) of 3 independent experiments. ∗P < .05. (D) As in panel A, except platelets were treated with either PP2 (20 μM), PP3 (20 μM), or dasatinib (10 μM) for 3 minutes before stimulation with oxLDL (50 μg/L; 15 seconds). Representative blots (upper) and densitometric analysis (lower) of 4 independent experiments. ∗P < .05. (E) As in panel A, except immunoblotted for Syk and FcRγ. Representative blots (upper) and densitometric analysis (lower) of 10 independent experiments. ∗P < .05. (F) As in panel A, except Syk was immunoprecipitated and immunoblotted for phospho-tyrosine, FcRγ, and Syk. Representative blots (upper) and densitometric analysis for phospho-Syk (lower-left) and FcRγ (lower-right) of 6 independent experiments. ∗P < .05. AU, arbitrary units; IB, immunoblot; IgG, immunoglobulin G; IP, immunoprecipitate.