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Characterization of the potentiation effect of activin on human erythroid
colony formation in vitro
J Yu, L Shao, J Vaughan, W Vale and AL Yu
Department of Molecular and Experimental Medicine, Research Institute of
Scripps Clinic, La Jolla, CA 92037.
Activin, also named FSH-releasing protein, was previously shown to induce
hemoglobin accumulation in K562 cells and potentiate the proliferation and
differentiation of CFU-E in human bone marrow cultures. Present studies
indicate that the potentiation effect of activin is lineage specific. In
addition to CFU-E, activin caused an increase in the colony formation of
BFU-E from either bone marrow or peripheral blood. It had little effect on
the colony formation of CFU- GM and the mixed colonies from CFU-GEMM. In
serum-depleted culture, the effect of activin was shown to be
dose-dependent with doses effective at picomolar concentrations. The
potentiation effect of activin was exerted indirectly through mediation of
both monocytes and T lymphocytes. Activin was also found to increase
specifically the proportion of DNA-synthesizing erythroid progenitors from
both bone marrow and peripheral blood. It had little effect on DNA
synthesis in CFU-GM and in mitogen-stimulated lymphocytes. Addition of the
monocytes or T lymphocytes to their respective depleted subpopulations of
mononuclear cells reconstituted the enhancing effect of activin on the
colony formation and DNA synthesis of erythroid progenitors. These results
strongly suggest a specific role of activin in potentiating the
proliferation and differentiation of erythroid progenitors in vitro.
Volume 73,
Issue 4,
pp. 952-960,
03/01/1989
Copyright © 1989 by The American Society of Hematology

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