Page 99 - Haematologica April 2020

GPX4 controls reticulocyte maturation
AB
CD
E
FGH
IJK
LM
Figure 3. Ineffective erythropoiesis in mice with Gpx4-deficiency in the hematopoietic system and severe aggravation by dietary vitamin E deficiency. Total numbers of bone marrow (BM) cells collected from (A) two femura and two tibiae and (B) spleen weights of wild-type (wt) mice (n=8) and of mice with Gpx4-deficient hematopoiesis maintained either on a normal (n=8) or a vitamin E-depleted diet (n=9). The total numbers of proerythroblasts and erythroblasts in the BM and spleen, and of reticulocytes and erythrocytes in the blood were assessed as described in the Online Supplementary Materials and Methods. Comparative quantification of the total numbers of (F-H) proerythroblasts ( n=8 for each condition), of (I-K) erythroblasts (n=8 for each condition), (L) reticulocytes and (M) erythrocytes (both n=42 wt; n=23 k.o., normal diet; n=16 k.o. minus vitE). Proerythroblasts in the BM and spleen were quantified separately in G and H, and erythroblasts in J and K, respec- tively. The significance was calculated by the Mann-Whitney test. The erythropenia caused by Gpx4-deficiency in hematopoietic cells is compensated to a large extent by increased extramedullary erythropoiesis and strongly elevated reticulocyte counts. Under combined Gpx4- and vitamin E-deficiency, the number or erythrocytes is strongly decreased, but the number of reticulocytes is not significantly higher than in wt mice. This points to a loss of erythroid progenitor cells at the proerythroblast and/or erythroblast stage in addition to the reticulocyte maturation defect under these conditions.
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