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Effects of dexamethasone on fetal hemoglobin synthesis in peripheral blood erythroid burst‐forming units
Author(s) -
Steinberg Martin H.,
Coleman Mary B.,
Garver Fred A.,
Grenett Hernan E.,
Pressley Annette,
Adams Junius G.
Publication year - 1981
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830100107
Subject(s) - fetal hemoglobin , dexamethasone , medicine , globin , endocrinology , sickle cell anemia , anemia , radioimmunoassay , hemoglobin , chemistry , fetus , biology , cell , immunology , biochemistry , pregnancy , genetics
Colonies derived from erythroid burst‐forming units (BFU‐E) synthesize fetal hemoglobin (HbF) in amounts that far exceed in vivo levels. There is some evidence that HbF synthesis is controlled at the level of a primitive erythroid precursor cell. Dexamethasone may potentiate the development of BFU‐E. Since a means of augmenting HbF production in sickle cell anemia or severe β‐thalassemia would be of great therapeutic value, we studied the effects of dexamethasone on HbF and γ‐globin chain synthesis in BFU‐E from patients with sickle cell anemia and controls. HbF was measured by radioimmunoassay of BFU‐E lysate and γ‐chain synthesis by the incorporation of 3 H‐leucine into globin, which was then purified by gel filtration and column chromatography. Dexamethasone (10 −9 M) produced an increase in the number of BFU‐E in 16 of 19 subjects when compared with numbers of BFU‐E cultured with only erythropoietin. The individual BFU‐E were larger and contained more subcolonies. Dexamethasone did not increase HbF or γ‐chain synthesis, and there was no relationship between increased proliferation of BFU‐E and augmented HbF production. Thus, although dexamethasone augmented the development of erythroid bursts, there was no increment in HbF.