Figure 3
Figure 3. Deficiency of both ActR2a and BMPR2 in hepatocytes induces iron overload. Serum iron levels (A) and transferrin saturations (B), as well as liver (C) and spleen (D) iron content, were measured in 10- to 12-week-old female control mice (ActR2a+/+;Bmpr2fl/fl [n = 7]) and mice globally deficient for ActR2a without or with hepatocyte-specific deletion of BMPR2 (ActR2a−/−;Bmpr2fl/fl [n = 23] and ActR2a−/−;Bmpr2fl/fl;Alb-Cre [n = 13], respectively). Mice carrying the Cre recombinase transgene are indicated by “Cre +”. ANOVAs P < .0001; *P < .0001 vs ActR2a+/+;Bmpr2fl/fl mice; #P < .0001 vs ActR2a−/−;Bmpr2fl/fl mice.

Deficiency of both ActR2a and BMPR2 in hepatocytes induces iron overload. Serum iron levels (A) and transferrin saturations (B), as well as liver (C) and spleen (D) iron content, were measured in 10- to 12-week-old female control mice (ActR2a+/+;Bmpr2fl/fl [n = 7]) and mice globally deficient for ActR2a without or with hepatocyte-specific deletion of BMPR2 (ActR2a−/−;Bmpr2fl/fl [n = 23] and ActR2a−/−;Bmpr2fl/fl;Alb-Cre [n = 13], respectively). Mice carrying the Cre recombinase transgene are indicated by “Cre +”. ANOVAs P < .0001; *P < .0001 vs ActR2a+/+;Bmpr2fl/fl mice; #P < .0001 vs ActR2a−/−;Bmpr2fl/fl mice.

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