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Effect of transforming growth factor-beta 1 on proliferation and induction
of hemoglobin accumulation in K-562 cells
LL Chen, A Dean, T Jenkinson and J Mendelsohn
Laboratory of Receptor Biology, Sloan-Kettering Institute, New York, NY.
The effects of transforming growth factor-beta 1 (TGF-beta 1) on
proliferation and hemoglobinization in K-562 cells, a human multipotential
hematopoietic cell line, were studied. We found that TGF- beta 1 could
induce hemoglobin accumulation in K-562 cells. Various clones were selected
on the basis of the inducibility of hemoglobinization by TGF-beta 1. One
high response clone (no. 1) and one low response clone (no. 8) were studied
in detail. Hemoglobin accumulation peaked on day 5 of culture in the
presence of TGF-beta 1 (0.5 ng/mL, 20 pmol/L), when 90% of clone 1 cells,
55% of parent line cells, and less than 10% of clone 8 cells contained
hemoglobin. There was a concomitant reduction in proliferation of 60% for
clone 1, 40% for the parent line, and 30% for the clone 8 on day 5 of
culture. Quantitative analysis showed that the hemoglobin contents in clone
1 after 5-day induction by TGF-beta 1 and hemin were 1.0 pg/cell and 2.9
pg/cell, respectively. The hemoglobin induced by TGF-beta 1 showed the same
electrophoretic characteristics as the hemoglobin induced by hemin. The
expression of epsilon-globin mRNA was minimally detectable in control cells
and was induced in both TGF-beta 1 and hemin treated cells. Other cytokines
with potential effects on K-562 cell proliferation and differentiation were
also studied. Interleukin-1, interleukin-3, interferon alpha, interferon
gamma, and inhibin, tested as single agents, showed minimal effects on
proliferation. None of these agents could induce hemoglobinization or
inhibit the hemoglobinization induced by TGF-beta 1.
Volume 74,
Issue 7,
pp. 2368-2375,
11/15/1989
Copyright © 1989 by The American Society of Hematology
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