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. 2005 Dec 5;202(11):1587–1597. doi: 10.1084/jem.20051108

Figure 4.

Figure 4.

Abnormal platelet function in Meg2/mice. (A) Images of platelet aggregates in response to ADP and thrombin. (a and b) Platelet-rich plasma from Meg2+/+ (a) and Meg2−/− (b) hematopoietic progenitor cell–transplanted mice was treated with 20 μM ADP. (c and d) Washed platelets from Meg2+/+ (c) and Meg2−/− (d) hematopoietic progenitor cell–transplanted mice were treated with 1 U/ml thrombin. (d) Note that the platelet aggregates from wild-type hematopoietic progenitor cell–transplanted mice are substantially larger than those derived from Meg2−/− mice. (B) Platelet aggregometry traces in response to thrombin and ADP. Left panel: platelet-rich plasma from Meg2+/+ (black trace) and Meg2−/− (gray trace) hematopoietic progenitor cell–transplanted mice was treated with thrombin to induce platelet aggregation. Platelet aggregation was measured by aggregometry after stimulation with 1 U/ml thrombin. Note the decreased thrombin-induced platelet aggregation in Meg2−/− platelets. Right panel: Washed platelets from Meg2+/+ (black trace) and Meg2−/− (gray trace) hematopoietic progenitor cell–transplanted mice (black trace) were treated with 20 μM ADP. Meg2−/− platelets demonstrate diminished platelet aggregation compared with Meg2+/+ platelets.