Fig. 2: ABT-737 treatment induces platelet apoptosis without causing desialylation.
From: Platelet aging and desialylation increase apoptotic priming and BCL-XL dependence

A Blood platelet count of WT and Asgr2–/– mice following a single intraperitoneal injection of ABT-737. Data collected from each mouse as well as mean is shown for n = 4–5 mice/group. Flow cytometry analysis of platelets collected from mice 90 min after ABT-737 injection using B Annexin V to detect apoptosis and C RCA-I lectin to detect exposed galactose. Mean ± SEM is shown for n = 3–4 biological replicates, as indicated by individual data points. D Percentage of circulating platelets: young (biotin−) and aged (biotin+) platelet populations in WT and Asgr2–/– mice 90 min after a single intraperitoneal injection of ABT-737 using biotinylation to compare young versus aged. Mean ± SEM is shown for n = 3 biological replicates. Flow cytometry analysis of platelets derived from WT mice after biotin (60 h) and ABT-737 (90 min) injections: E Annexin V to detect apoptosis, and F RCA-I lectin to detect exposed galactose. Mean ± SEM is shown for n = 2–3 biological replicates. Flow cytometry analysis of freshly washed WT platelets treated with neuraminidase (1 μM) or ABT-737 (5 μM) for 20 min in vitro at 37 °C using G RCA-I to detect exposed galactose and H Annexin V to detect apoptosis. Mean ± SEM is shown for n = 2–4 biological replicates, as indicated by individual data points.