Figure 1
Figure 1. Agonist-dependent modulation of platelet aggregation of SR-BI−/−–deficient mice. (A-F) Platelet aggregation in PRP from WT and SR-BI−/− mice was induced by selective PAR4-AP, ADP, or convulxin and was optically monitored. (B,D,F) Representative aggregation curves in response to PAR4-AP (60μM to 150μM; B), or ADP (1μM; D), or convulxin (500 ng/mL; F) are shown, respectively. (A,C,E) Quantifications of the aggregation data are expressed as maximal amplitude of aggregation within 5 minutes after adding the agonist (mean ± SEM), and data are presented as a typical result of at least 3 independent experiments. *P < .05, **P < .01.

Agonist-dependent modulation of platelet aggregation of SR-BI−/−–deficient mice. (A-F) Platelet aggregation in PRP from WT and SR-BI−/− mice was induced by selective PAR4-AP, ADP, or convulxin and was optically monitored. (B,D,F) Representative aggregation curves in response to PAR4-AP (60μM to 150μM; B), or ADP (1μM; D), or convulxin (500 ng/mL; F) are shown, respectively. (A,C,E) Quantifications of the aggregation data are expressed as maximal amplitude of aggregation within 5 minutes after adding the agonist (mean ± SEM), and data are presented as a typical result of at least 3 independent experiments. *P < .05, **P < .01.

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