Figure 3.
Figure 3. oxLDL-mediated platelet PSer exposure requires CD36 signaling through the redox sensor MAPK ERK5. Human platelets (1 × 108/mL) were pretreated with 1 μg/mL CD36 blocking antibody FA6-152 or nonimmunizing IgG isotype control (A), 2000 U/mL denatured boiled PEG catalase or native PEG catalase (B), 10 μM Src kinase inhibitor PP2, or control analog inhibitor PP3, 10 μM MEK5/ERK5 inhibitor BIX 02188 or JNK inhibitor SP600125 (C) or the indicated concentrations (D). Percent-positive annexin V binding was measured by flow cytometry after 50 μg/mL oxLDL only in panels A-C or 50 μg/mL oxLDL in the presence of 500 ng/mL CVX in panel D. Data represented as mean ± SEM and analyzed by 1-way ANOVA with Tukey post hoc analysis. *P < .05 compared to oxLDL with CVX in panel D. N of 4 different donors in panel A; 4 different donors in panel B; >3 donors in panel C; and 3 different donors in panel D.

oxLDL-mediated platelet PSer exposure requires CD36 signaling through the redox sensor MAPK ERK5. Human platelets (1 × 108/mL) were pretreated with 1 μg/mL CD36 blocking antibody FA6-152 or nonimmunizing IgG isotype control (A), 2000 U/mL denatured boiled PEG catalase or native PEG catalase (B), 10 μM Src kinase inhibitor PP2, or control analog inhibitor PP3, 10 μM MEK5/ERK5 inhibitor BIX 02188 or JNK inhibitor SP600125 (C) or the indicated concentrations (D). Percent-positive annexin V binding was measured by flow cytometry after 50 μg/mL oxLDL only in panels A-C or 50 μg/mL oxLDL in the presence of 500 ng/mL CVX in panel D. Data represented as mean ± SEM and analyzed by 1-way ANOVA with Tukey post hoc analysis. *P < .05 compared to oxLDL with CVX in panel D. N of 4 different donors in panel A; 4 different donors in panel B; >3 donors in panel C; and 3 different donors in panel D.

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