Figure 3
Requirement of PKC for oxidative platelet particle formation induced by PMA (activates PKC). (A) Catalase and DPI inhibit PMA-induced (200 nM) platelet particle formation. C1 and C2 represent control buffer and control IgG. Pt is patient Ab. Catalase and DPI lanes are as in Figure 2A, with lane 0 as PMA alone (n=4). (B) PMA-induced platelet particle formation requires the NADPH oxidase pathway (same designations as in Figure 2B). (C) PMA-induced platelet particle formation requires 12-LO (same designations as in Figure 2C). (D) PMA-induced platelet particle formation (200 nM) is inhibited by the PKC inhibitor bisindolylmaleimide. Ctl and Ctlb are respective controls for patient IgG and PMA, respectively. Lanes, 1, 2, and 3 refer to doubling PKC inhibitor concentrations starting at 100 μM (n=4). SEM is given.

Requirement of PKC for oxidative platelet particle formation induced by PMA (activates PKC). (A) Catalase and DPI inhibit PMA-induced (200 nM) platelet particle formation. C1 and C2 represent control buffer and control IgG. Pt is patient Ab. Catalase and DPI lanes are as in Figure 2A, with lane 0 as PMA alone (n=4). (B) PMA-induced platelet particle formation requires the NADPH oxidase pathway (same designations as in Figure 2B). (C) PMA-induced platelet particle formation requires 12-LO (same designations as in Figure 2C). (D) PMA-induced platelet particle formation (200 nM) is inhibited by the PKC inhibitor bisindolylmaleimide. Ctl and Ctlb are respective controls for patient IgG and PMA, respectively. Lanes, 1, 2, and 3 refer to doubling PKC inhibitor concentrations starting at 100 μM (n=4). SEM is given.

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