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. 2009 Feb 13;113(24):6051–6060. doi: 10.1182/blood-2008-07-170571

Figure 5.

Figure 5

Effect of polyclonal anti–GPIIIa49-66 or rADAMTS-18 385-AA fragment (AD-18F) on disaggregation and destruction of ex vivo platelet aggregates and anti–ADAMTS-18 Ab on in vivo bleeding time. (A) Collagen platelet aggregate. Ctl (scrambled [sc] ADAMTS-18F or 66-AA fragments), PtIgG (patient anti–GPIIIa49-66), media, and AD-18F were incubated with aggregates for 0.5, 1, 2, 4, and 8 hours at 37°C. The numbers of platelets/aggregate were then counted. Note that both AD-18F and anti–GPIIIa49-66 have a similar kinetic effect, representative of 3 experiments. (B) Photomicrograph of platelet collagen aggregates before and after treatment with anti–GPIIIa49-66 or control (scAD-18F or 66-AA fragment). (C) Effect of prestimulated platelet PAR-1 on induction of platelet fragmentation with AD-18F. Gel-filtered platelets were treated with the PAR-1 agonist TFLLRN (200 μM) for 30 minutes at 37°C and then followed with various AD-18F concentrations (50-6 μg/mL) for 4 hours. Inline graphic and ■ are without and with TFLLRN (T) prestimulation, respectively. Note increased sensitivity of activated platelets to AD-18F at low AD-18F concentration. Error bars indicate SEM. (D) Effect of polyclonal anti–ADAMTS-18 Ab on mouse bleeding time. BALB/C mice were injected intravenously with 10 μg anti–ADAMTS-18 IgG (AD-IgG) or preimmune IgG (PIS-IgG) and their bleeding time was monitored 60 minutes later (n = 10).