Figure 6.
Romiplostim rescues platelet reactivity in G6b-deficient mice. Washed platelet aggregation and ATP secretion of WT and G6b KO mice before and after 21 days after romiplostim administration were measured using lumi-aggregometry in response to (A-B) 30 and 3 μg/mL collagen-related peptide (CRP), (C) 3 μg/mL collagen, (D) 3 μg/mL CLEC2 Ab and (E) 0.06 U/mL thrombin. Following romiplostim administration, platelets from G6b KO mice aggregated normally in response to 30 μg/mL CRP and 3 μg/mL collagen, compared with treated WT mice (A,C) and an increased response to 3 μg/mL CRP was observed in treated vs untreated G6b KO mouse platelets (B). Romiplostim treatment also partially attenuates the response of WT and G6b KO platelets to anti-CLEC-2 antibody (D) and fully restores reversible aggregation and reduced ATP secretion in response to 0.06 U/mL thrombin in G6b KO mice (E). Representative traces are shown, n = 5 to 8 mice per genotype per condition.

Romiplostim rescues platelet reactivity in G6b-deficient mice. Washed platelet aggregation and ATP secretion of WT and G6b KO mice before and after 21 days after romiplostim administration were measured using lumi-aggregometry in response to (A-B) 30 and 3 μg/mL collagen-related peptide (CRP), (C) 3 μg/mL collagen, (D) 3 μg/mL CLEC2 Ab and (E) 0.06 U/mL thrombin. Following romiplostim administration, platelets from G6b KO mice aggregated normally in response to 30 μg/mL CRP and 3 μg/mL collagen, compared with treated WT mice (A,C) and an increased response to 3 μg/mL CRP was observed in treated vs untreated G6b KO mouse platelets (B). Romiplostim treatment also partially attenuates the response of WT and G6b KO platelets to anti-CLEC-2 antibody (D) and fully restores reversible aggregation and reduced ATP secretion in response to 0.06 U/mL thrombin in G6b KO mice (E). Representative traces are shown, n = 5 to 8 mice per genotype per condition.

Close Modal

or Create an Account

Close Modal
Close Modal