Figure 6.
Figure 6. PECAM-1–deficient platelets display normal soluble FITC-fibrinogen binding and JON/A PE binding following treatment with thrombin, PAR-4 peptide, ADP, ADP in synergy with epinephrine, and CRP. (A) FACS analysis of FITC-conjugated fibrinogen binding to platelets stimulated with thrombin (1 U/mL), PMA (20 μM), ADP (10 μM), ADP (10 μM) + epinephrine (20 μM), or unstimulated (control). Results are cumulative data from 3 independent assays and are presented as geometric mean fluorescence intensity (GMFI) ± SEM. (B-C) Flow cytometric analysis of JON/A-PE mAb binding to platelets stimulated with 0 to 1.0 U/mL thrombin, 0 to 250 μM PAR-4 agonist peptide, 2.5 to 10 μg/mL CRP, 10 μM ADP with or without 20 μM epinephrine, or unstimulated (control). Results are cumulative data from 3 independent experiments and are presented as geometric mean fluorescence intensity (GMFI) ± SEM.

PECAM-1–deficient platelets display normal soluble FITC-fibrinogen binding and JON/A PE binding following treatment with thrombin, PAR-4 peptide, ADP, ADP in synergy with epinephrine, and CRP. (A) FACS analysis of FITC-conjugated fibrinogen binding to platelets stimulated with thrombin (1 U/mL), PMA (20 μM), ADP (10 μM), ADP (10 μM) + epinephrine (20 μM), or unstimulated (control). Results are cumulative data from 3 independent assays and are presented as geometric mean fluorescence intensity (GMFI) ± SEM. (B-C) Flow cytometric analysis of JON/A-PE mAb binding to platelets stimulated with 0 to 1.0 U/mL thrombin, 0 to 250 μM PAR-4 agonist peptide, 2.5 to 10 μg/mL CRP, 10 μM ADP with or without 20 μM epinephrine, or unstimulated (control). Results are cumulative data from 3 independent experiments and are presented as geometric mean fluorescence intensity (GMFI) ± SEM.

Close Modal

or Create an Account

Close Modal
Close Modal