Fig. 1.
Fig. 1. Survival of in vivo biotinylated wild-type and P-selectin–deficient platelets. Blood from mice of both genotypes was in vivo biotinylated as described in Materials and Methods. The percentage of biotinylated cells present at various time intervals after biotinylation was determined by flow cytometry. Because the absolute levels of biotinylated platelets varied among mice, the least square-fitted curve for each mouse was normalized with respect to their value at time zero (% of biotinylated platelets and red blood cells at time zero = 100). Each curve represents a composite curve and linear fit (r = 0.99) for the data of eight mice in each genotype. Superimposed curves were obtained with wild-type (P-sel+/+) (△) and P-selectin–deficient (P-sel-/-) (◊) platelets with a mean life span of 4.72 ± 0.32 and 4.71 ± 0.3 days, respectively. Red blood cells from wild-type animals (◍) were used as a control for the stability of the biotinylation.

Survival of in vivo biotinylated wild-type and P-selectin–deficient platelets. Blood from mice of both genotypes was in vivo biotinylated as described in Materials and Methods. The percentage of biotinylated cells present at various time intervals after biotinylation was determined by flow cytometry. Because the absolute levels of biotinylated platelets varied among mice, the least square-fitted curve for each mouse was normalized with respect to their value at time zero (% of biotinylated platelets and red blood cells at time zero = 100). Each curve represents a composite curve and linear fit (r = 0.99) for the data of eight mice in each genotype. Superimposed curves were obtained with wild-type (P-sel+/+) (△) and P-selectin–deficient (P-sel-/-) (◊) platelets with a mean life span of 4.72 ± 0.32 and 4.71 ± 0.3 days, respectively. Red blood cells from wild-type animals (◍) were used as a control for the stability of the biotinylation.

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