Figure 3
Figure 3. The rabbit anti-ERP57 Ab 1 preferentially inhibits platelet aggregation. (A) The effect of Ab 1 and 2 are seen in representative tracings of platelet aggregation induced with (i) collagen and (ii) SFLLRN. (B) The combined data ± SE of at least 3 independent experiments is shown for collagen and SFLLRN. (C) The binding of Ab1 to resting platelets relative to normal IgG (i) with the cumulative results ± SE of a gated population of platelets also shown (ii; n = 8). (D) Anti-ERp57 (Ab1) inhibits SFLLRN (10μM)–induced PAC1 binding when added before (i), but not after (ii), activation. (i) PAC1 binding to nonactivated platelets (NA) is seen on the left. (iii) Inhibition of PAC1 binding by Ab1 as the percentage of fluorescent intensity relative to the normal rabbit IgG control, ± SE (n = 4). (E) A representative histogram (i) and combined data (ii) show that Ab1 inhibits P-selectin binding to convulxin (10 ng/mL)–activated platelets relative to normal IgG ± SE (n = 5). In these experiments, the Abs (30 μg/mL) were incubated with the platelets for 10 minutes before the addition of the agonist.

The rabbit anti-ERP57 Ab 1 preferentially inhibits platelet aggregation. (A) The effect of Ab 1 and 2 are seen in representative tracings of platelet aggregation induced with (i) collagen and (ii) SFLLRN. (B) The combined data ± SE of at least 3 independent experiments is shown for collagen and SFLLRN. (C) The binding of Ab1 to resting platelets relative to normal IgG (i) with the cumulative results ± SE of a gated population of platelets also shown (ii; n = 8). (D) Anti-ERp57 (Ab1) inhibits SFLLRN (10μM)–induced PAC1 binding when added before (i), but not after (ii), activation. (i) PAC1 binding to nonactivated platelets (NA) is seen on the left. (iii) Inhibition of PAC1 binding by Ab1 as the percentage of fluorescent intensity relative to the normal rabbit IgG control, ± SE (n = 4). (E) A representative histogram (i) and combined data (ii) show that Ab1 inhibits P-selectin binding to convulxin (10 ng/mL)–activated platelets relative to normal IgG ± SE (n = 5). In these experiments, the Abs (30 μg/mL) were incubated with the platelets for 10 minutes before the addition of the agonist.

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