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Proliferation and differentiation of myelodysplastic CD34+ cells:
phenotypic subpopulations of marrow CD34+ cells
K Sawada, N Sato, A Notoya, T Tarumi, S Hirayama, H Takano, K Koizumi, T Yasukouchi, M Yamaguchi and T Koike
Department of Medicine II, Hokkaido University School of Medicine, Sapporo,
Japan.
In a search for a mechanism to explain the impaired growth of progenitor
cells in patients with myelodysplastic syndromes (MDS), marrow CD34+ cells
were purified up to 94.9% +/- 4.2% for normal individuals and 88.1% +/-
17.6% for MDS patients, using monoclonal antibodies and immunomagnetic
microspheres (MDS CD34+ cells). Phenotypic subpopulations of these CD34+
cells were analyzed for CD38, HLA-DR, CD33, CD13, CD14, CD41 and CD3 plus
CD19, in association with proliferative and differentiative capacities. The
15 studies performed included 12 MDS patients. Coexpression rate of CD13
significantly increased in the MDS CD34+ cell population with a value of
91.4% +/- 11.6% and ranging from 60.3% to 100%, and exceeded 99% in four
studies, whereas that of normal CD34+ cells was 49.9% +/- 15.8%, ranging
from 28.2% to 70.1% (P < .001). Coexpression rate of CD38, HLA-DR, CD33,
CD14, and CD3 plus CD19 in MDS CD34+ cells did not significantly differ
from that of normal CD34+ cells. The total number of colonies and clusters
grown from 100 normal marrow CD34+ cells was 40.4 +/- 8.6, the range being
from 27.2 to 50.3; this varied in MDS marrow CD34+ cells with a value of
34.0 +/- 28.7, the range being 0 to 95.9. The lineage of colonies and
clusters promoted by MDS marrow CD34+ cells was predominantly committed to
nonerythroid with impaired differentiation in 13 of 15 studies (87%). CD13
is first expressed during hematopoiesis by colony-forming unit
granulocyte-macrophage and is absent in erythroid progenitors. Therefore,
this study provides direct evidence for the lineage commitment of MDS CD34+
cells to nonerythroid with impaired differentiation and explains the
mechanism of nil or low colony expression of MDS progenitor cells to
erythroid lineage.
Volume 85,
Issue 1,
pp. 194-202,
01/01/1995
Copyright © 1995 by The American Society of Hematology
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