Figure 1.
Figure 1. Demonstration of the role of VWF in platelet FVIII level and activity. (A) Antigenic determination of hB-FVIII in platelet releasate compared with a standard curve using recombinant hB-FVIII.2 Platelets were from transgenic hB-FVIII/FVIIInull mice that were also either wild type (WT; +/+), heterozygote (+/-), or homozygote (-/-) for the VWF targeted gene deletion as noted in the graph. Means ± 1 standard deviation (SD) are shown. (B) WBCT studies were determined as previously described.2 Studied animals are as in panel A. Means ± 1 standard deviation (SD) are shown. WBCT in WT mice is 5.0 ± 1.0 minute and greater than 45 minutes in FVIIInull mice. (C) Carotid artery FeCl3 injury studies as previously described.10 A representative thrombosis curve for each platelet-donor phenotype (top row) and for the FVIIInull/VWF+/+ recipient mice (center) is shown. Similar curves for posttransfusion recipient animals are shown (bottom row). Each group was studied 5 or more times with similar results.

Demonstration of the role of VWF in platelet FVIII level and activity. (A) Antigenic determination of hB-FVIII in platelet releasate compared with a standard curve using recombinant hB-FVIII. Platelets were from transgenic hB-FVIII/FVIIInull mice that were also either wild type (WT; +/+), heterozygote (+/-), or homozygote (-/-) for the VWF targeted gene deletion as noted in the graph. Means ± 1 standard deviation (SD) are shown. (B) WBCT studies were determined as previously described. Studied animals are as in panel A. Means ± 1 standard deviation (SD) are shown. WBCT in WT mice is 5.0 ± 1.0 minute and greater than 45 minutes in FVIIInull mice. (C) Carotid artery FeCl3 injury studies as previously described.10  A representative thrombosis curve for each platelet-donor phenotype (top row) and for the FVIIInull/VWF+/+ recipient mice (center) is shown. Similar curves for posttransfusion recipient animals are shown (bottom row). Each group was studied 5 or more times with similar results.

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