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Enhanced Megakaryocyte and Erythroid Development From Normal
Human CD34+ Cells: Consequence of Enforced Expression of
SCL
Ngaire J. Elwood,
Helen Zogos,
Daniel S. Pereira,
John E. Dick, and
C. Glenn Begley
From the Rotary Bone Marrow Research Laboratories and the Walter and
Eliza Hall Institute of Medical Research, Royal Melbourne Hospital,
Parkville, Victoria, Australia; the Department of Genetics, Research
Institute, Hospital for Sick Children, and the Department of Molecular
and Medical Genetics, University of Toronto, Toronto, Ontario, Canada.
The product of the SCL gene is a basic helix-loop-helix (bHLH)
transcription factor that is essential for the development of
hematopoietic stem cells in both the embryo and the adult. However,
once the stem cell compartment is established, the function of SCL in
subsequent differentiation and commitment events within normal
hematopoietic cells remains undefined. The aim of the current study was
to investigate this role using purified normal human hematopoietic
CD34+ cells. An SCL retrovirus was used to transduce
CD34+ cells isolated from human bone marrow, peripheral
blood, and umbilical cord blood. Enforced expression of SCL increased
by a median of twofold the number of erythroid colonies, with an increase in both colony size and the rate of hemoglobinization. Unexpectedly, enforced expression in CD34+ cells also
significantly increased the number of megakaryocyte colonies, but with
no impact on the size of colonies. There was no consistent effect on
the number nor size of granulocyte-macrophage (GM) colonies. The
proliferative effect of enforced SCL expression on erythroid cells was
attributed to a shortened cell cycle time; the self-renewal capacity of
erythroid or GM progenitors was unchanged, as was survival of cells
within colonies. These results demonstrate a role for SCL in
determining erythroid and megakaryocyte differentiation from normal
human hematopoietic CD34+ cells.
Blood, Vol. 91 No. 10 (May 15), 1998:
pp. 3756-3765
© 1998 by The American Society of Hematology.
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