Thromboregulatory manifestations in human CD39 transgenic mice and the implications for thrombotic disease and transplantation
J. Clin. Invest. Karen M. Dwyer, et al. 113:1440 doi:10.1172/JCI19560 [Go to this article.]

Figure 2
Expression of hCD39 in transgenic mice affects hemostasis and platelet function. (A) Platelet aggregation studies. The presence of hCD39 on the surface of platelets altered the responsiveness of platelets to agonists ADP and collagen. The initial response to both ADP and collagen was attenuated; however, a complete aggregatory response was subsequently demonstrated. Data shown are representative of three different experiments. (B) Tail-bleeding times. Expression of hCD39 significantly prolonged time to hemostasis compared with WT mice either untreated or treated with apyrase. Treatment with apyrase prolonged bleeding compared with WT control. (C) Tail-bleeding times in the adoptive transfer experiments. The presence of hCD39 either on the endothelium or blood components alone was sufficient to induce a bleeding diathesis. Experiments using transgenic mice were terminated (*) at 15 minutes to prevent hemorrhagic death. Data represent mean ± SEM for six mice in each group. IRR, irradiated. (D) Whole blood aggregation. In response to collagen, WT blood (solid line) aggregated normally. This response was completely abolished in whole blood from mice transgenic for hCD39 (broken line).