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We studied the relation between ferritin cellular binding and suppressive activity of recombinant H- and L-ferritin on human erythroid cells at different proliferation/differentiation phases. L-ferritin failed to show any suppressive activity or detectable binding to erythroblasts at any stage of maturation. In contrast, H-ferritin demonstrated binding to erythroblasts derived from peripheral BFU-E cells which increased steadily between 7-14 days of culture up to 15,000 molecules per cell. Reticulocytes and erythrocytes failed to bind either L- or H-ferritin. H-ferritin suppressed BFU-E colony formation and reduced K562 cell proliferation at nanomolar concentrations. This suggests that the expression of H-ferritin binding sites is modulated by cellular proliferation and differentiation, that cells expressing H-ferritin binding sites are sensitive to ferritin suppressive activity and that a causal relation exists between ferritin cellular binding and suppressive activity.

Variations in the number of peripheral burst-forming unit--erythroid (BFU-E) of healthy women were observed during a prolonged period of observation. These differences were related to different phases of the menstrual cycle. A peak in the number of BFU-E occurred on day 14 of the cycle corresponding to the serum 17-beta-estradiol peak. The effect of estrogens and progesterone on the in vitro growth of peripheral BFU-E of healthy women was assayed. Estrogens demonstrated a stimulatory and progesterone an inhibitory effect in total lymphomonocyte cultures, whereas neither hormone had an effect in monocyte-depleted cultures. Prostaglandin E1 (PGE1) which is known to be secreted by monocytes, stimulated the in vitro growth of peripheral BFU-E. These data suggest that estrogens and progesterone could have a role in the in vitro growth of peripheral BFU-E, probably mediated by monocytes.