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. 2019 Nov 23;4(1):50–65. doi: 10.1002/hep4.1440

Figure 4.

Figure 4

HNA2 induces platelet aggregation and activation. (A) Platelets were incubated with ex vivo prepared HMA (1 mg/mL), HNA1 (1 mg/mL), and HNA2 (1 mg/mL), and aggregation was induced with collagen (0.2 μg/mL). Representative reading and bar graph indicate increased aggregation in HNA2‐treated platelets as compared with HNA1 and HMA. Data are expressed as percent of normalized platelet aggregation (n = 3). (B) CD40L and ROS production in healthy platelets was significantly increased when exposed to HNA2 (1 mg/mL). Pretreatment with anti‐CD36 blocking antibody (1 μg/mL) significantly reverses the effect, particularly in HNA2‐exposed platelets. (C) EGTA decreases HNA2‐induced platelet expression of CD40L and ROS production in a dose‐dependent manner. Platelets were pre‐incubated with EGTA, and activation was induced with HNA2 (1 mg/mL). (D) Histogram represents the percent expression of platelets exposed to HNA2 (1 mg/mL) showing increased expression of P‐selectin, PAC‐1, and intracellular calcium as compared with HNA1 (n = 5). (E) Expression of SNARE complex proteins (Syntaxin‐11, SNAP‐23, and VAMP‐8) increases in healthy platelets exposed to HNA2 (1 mg/mL) as compared with HNA1 and HMA. Interestingly, anti‐CD36 blocking antibody (1 μg/mL) reduced the effect of HNA2 over others. Results expressed as mean ± SEM (*P < 0.05, **P < 0.01, ***P < 0.001).