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. 2021 May 18;10:e68217. doi: 10.7554/eLife.68217

Figure 5. ERFE loss in β-thalassemia mice causes profound bone loss.

(A) Bone mineral density (BMD) measured in whole body, femur, tibia, and lumbar spine (L4–L6) in 5-month-old β-thalassemia mice (Hbbth3/+ mice) and compound Hbbth3/+;Erfe-/- mutants. (B) Representative section of femoral epiphyses stained with Von Kossa, and quantitative estimates of bone volume (BV/TV) and trabecular thickness (Tb.Th). (C) Dynamic histomorphometry following two i.p. injections of calcein (green) and xylenol orange (red) given at days 8 and 2, respectively. Shown are measured and derived parameters, namely mineralizing surface (MS), mineral apposition rate (MAR) and bone formation rate (BFR). (D) Representative image of TRAP (ACP5) staining of femoral epiphysis, also showing both osteoclast surface (Oc.S) and number (N.Oc), expressed as a function of bone surface (BS). Statistics: Mean ± SEM; unpaired two-tailed Student’s t-test; *p<0.05, **p<0.01; N = 4–5 mice per group.

Figure 5.

Figure 5—figure supplement 1. Erythropoiesis-related parameters in Hbbth3/+ and Hbbth3/+;Erfe-/-mutant mice.

Figure 5—figure supplement 1.

We confirm previously reported differences in relative to wild-type (WT) mice with decreased red blood cell (RBC) count (A), hemoglobin (B), and mean corpuscular hemoglobin (MCH) (C) as well as increased reticulocyte count (D), spleen weight (E), and bone marrow erythroblast fraction (F) with only minor differences in RBC count and hemoglobin between Hbbth3/+ and compound Hbbth3/+;Erfe-/- mutant mice. Statistics: Mean ± SEM; unpaired two-tailed Student's ttest; *p<0.05, **p<0.01, ***p<0.0001; N = 4–5 mice per group.