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An autocrine role for erythropoietin in mouse hematopoietic cell
differentiation [published erratum appears in Blood 1992 Jun
15;79(12):3397]
O Hermine, N Beru, N Pech and E Goldwasser
Department of Biochemistry and Molecular Biology, University of Chicago, IL
60637.
Erythropoietin (epo) is the primary regulator of the rate of red blood cell
formation in mammals. Because it is formed in the kidney and acts on the
bone marrow, its action is classically endocrine. We have shown by PCR that
marrow cells contain epo mRNA and that antisense oligodeoxynucleotides, to
both epo and its receptor, act on multipotent hematopoietic cells to cause
a decrease in mixed erythroid:nonerythroid colonies. The antisense
oligonucleotides also cause an increase in mixed nonerythroid colonies with
no effect on erythroid burst formation. Sense oligonucleotides have no
effect. The antisense suppression is not due to adherent cells, cycling
late differentiated cells or lymphocytes, and not reversed by exogenous
epo. We conclude that normal erythroid differentiation may have an early
phase that is dependent on an internal autocrine mechanism involving epo
and its receptor.
Volume 78,
Issue 9,
pp. 2253-2260,
11/01/1991
Copyright © 1991 by The American Society of Hematology
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