Figure 1.
OxLDL increases platelet intracellular O2•−and H2O2 to promote platelet aggregation. 2-OH-E+ was detected by HPLC after washed human platelets (6 × 108/mL) were stimulated with varying concentrations of oxLDL for 45 minutes (A) (n = 3) over the course of time with buffer, native LDL (50 µg/mL), or oxLDL (50 µg/mL) (B) (n = 3), and after oxLDL stimulation in the presence of CD36 blocking antibody FA6-152 or control IgG antibody (1 µg/mL) (C) (n = 4). Platelet aggregation by oxLDL was measured over time after washed human platelets were treated with NOX inhibitor VAS2870 or DMSO control (5 or 10 µM) (n = 3) (D-E) in the presence or absence of buffer, PEG-catalase (1000 U/mL), or boiled PEG-catalase (1000 U/mL) (F) (n = 4). Data represented as mean ± standard error of the mean (SEM). P value determined by 1-way analysis of variance (ANOVA) with Dunnett post hoc multiple comparisons analysis (A), 2-tailed Student t test (C-D), and 1-way ANOVA with Tukey post hoc multiple comparisons analysis (B,E-F).

OxLDL increases platelet intracellular O2•−and H2O2 to promote platelet aggregation. 2-OH-E+ was detected by HPLC after washed human platelets (6 × 108/mL) were stimulated with varying concentrations of oxLDL for 45 minutes (A) (n = 3) over the course of time with buffer, native LDL (50 µg/mL), or oxLDL (50 µg/mL) (B) (n = 3), and after oxLDL stimulation in the presence of CD36 blocking antibody FA6-152 or control IgG antibody (1 µg/mL) (C) (n = 4). Platelet aggregation by oxLDL was measured over time after washed human platelets were treated with NOX inhibitor VAS2870 or DMSO control (5 or 10 µM) (n = 3) (D-E) in the presence or absence of buffer, PEG-catalase (1000 U/mL), or boiled PEG-catalase (1000 U/mL) (F) (n = 4). Data represented as mean ± standard error of the mean (SEM). P value determined by 1-way analysis of variance (ANOVA) with Dunnett post hoc multiple comparisons analysis (A), 2-tailed Student t test (C-D), and 1-way ANOVA with Tukey post hoc multiple comparisons analysis (B,E-F).

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