Figure 2
Figure 2. ODSH inhibits PF4/heparin complex binding to platelets in a mixture with UFH dependent on platelet activation. ODSH reduced PF4/heparin complex binding even if incubated concurrently with UFH (filled symbols). In case of activated platelets, higher ODSH concentrations are needed for inhibition (open symbols). GFPs were incubated with 25 μg/mL PF4 in the presence of 0.52 μg/mL UFH and increasing concentrations of ODSH concurrently (filled symbols). In addition, platelets were first incubated with 4 μg/mL abciximab and then incubated with 25 μg/mL PF4 in the presence of 0.52 μg/mL UFH, increasing concentrations of ODSH, and 100 ng/mL convulxin (open symbols). PF4 binding was detected with a FITC-labeled anti–human PF4 Ab using flow cytometry and Ab binding was quantified by geometric MFI. PF4 binding in the presence of PF4 and UFH alone was defined as 100%. Data are mean ± SD of at least 3 independent experiments.

ODSH inhibits PF4/heparin complex binding to platelets in a mixture with UFH dependent on platelet activation. ODSH reduced PF4/heparin complex binding even if incubated concurrently with UFH (filled symbols). In case of activated platelets, higher ODSH concentrations are needed for inhibition (open symbols). GFPs were incubated with 25 μg/mL PF4 in the presence of 0.52 μg/mL UFH and increasing concentrations of ODSH concurrently (filled symbols). In addition, platelets were first incubated with 4 μg/mL abciximab and then incubated with 25 μg/mL PF4 in the presence of 0.52 μg/mL UFH, increasing concentrations of ODSH, and 100 ng/mL convulxin (open symbols). PF4 binding was detected with a FITC-labeled anti–human PF4 Ab using flow cytometry and Ab binding was quantified by geometric MFI. PF4 binding in the presence of PF4 and UFH alone was defined as 100%. Data are mean ± SD of at least 3 independent experiments.

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