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. Author manuscript; available in PMC: 2015 Jan 1.
Published in final edited form as: Nat Genet. 2014 Jun 1;46(7):678–684. doi: 10.1038/ng.2996

Figure 5. Fam132b-deficient mice do not suppress hepcidin in response to phlebotomy and show delayed recovery from anemia.

Figure 5

(A) After phlebotomy, hepatic Hamp mRNA expression was measured in Fam132b+/+ (dashed line), Fam132b+/− (dotted line) and Fam132b−/− (solid line) littermates (n=6 to 14 per genotype and time-point). Hepcidin is suppressed after hemorrhage in wild-type mice but not in Fam132b-deficient mice, with Fam132b+/− presenting an intermediate response between the wild-types and knockouts. (B) After phlebotomy, both Fam132b+/+ (dashed line) and Fam132b+/− (dotted line) mice increase Fam132b mRNA expression in the bone marrow, although the maximal levels were about twice as high in Fam132b+/+ compared to Fam132b+/−. (C and D) Phlebotomized Fam132b-deficient mice (solid line) compared to wild-type mice (dashed line) showed delayed recovery of hemoglobin and lower mean corpuscular hemoglobin (MCH). Hepcidin (Hamp) (A) and Fam132b (B) mRNA levels were measured by qRT-PCR and shown as −ΔCt (i.e., Ct Hprt – Ct Hamp or Fam132b). For each genotype, means of −ΔCt values were compared at each time-point to the respective control mice t=0 by two-tailed Student t-test. Hematological parameters (C, D) were compared for each measurement between WT (n=17) and KO (n=15) by Student t-test. All graphs show means ± SEM. In the absence of gender differences, the genders were combined for each parameter. ***p<0.001, **p<0.01, *p<0.05