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Differential expression of transforming growth factor-beta, basic
fibroblast growth factor, and their receptors in CD34+ hematopoietic
progenitor cells from patients with myelofibrosis and myeloid metaplasia
MC Le Bousse-Kerdiles, S Chevillard, A Charpentier, N Romquin, D Clay, F Smadja-Joffe, V Praloran, B Dupriez, JL Demory, C Jasmin and MC Martyre
INSERM U268, Hopital Paul Brousse, Villejuif, France.
Myelofibrosis with myeloid metaplasia (MMM) is a myeloproliferative
disorder characterized by clonal expansion of hematopoiesis and marrow
fibrosis. Previous results from our group have shown an increased
production of two potent fibrogenic factors also involved in the regulation
of primitive hematopoietic cells, namely transforming growth factor-beta1
(TGF-beta1) and basic fibroblast growth factor (bFGF), in patients with
MMM. It is likely to assume that the myeloproliferation characteristic of
this disease may result from an abnormal proliferation of CD34+
hematopoietic progenitors. Thus, we were particularly concerned in studying
the gene and protein expression of these cytokines and their receptors in
CD34+ progenitors purified from the peripheral blood of MMM patients by
using semiquantitative reverse transcriptase-polymerase chain reaction and
immunolabeling methods. Our data showed that the expression of TGF-beta1 is
not altered in patients CD34+ cells; in contrast, the expression of
TGF-beta type II receptor is significantly decreased in such cells, as
compared with CD34+ cells from healthy subjects. Regarding bFGF, the very
low expression of the cytokine and its type I and II receptors detected in
normal CD34+ cells contrasts with that observed in patients' CD34+ cells,
which is significantly higher. Our results might be a clue for a better
understanding of the mechanism(s) involved in the dysregulation of
hematopoiesis in MMM. Actually, the increased expression of bFGF and its
receptors associated with the reduction of the TGF-beta binding receptor in
CD34+ progenitors from MMM patients might facilitate the expansion of
hematopoietic progenitors, not only by stimulating their growth and/or
survival, but also by overcoming negative regulatory signals.
Volume 88,
Issue 12,
pp. 4534-4546,
12/15/1996
Copyright © 1996 by The American Society of Hematology
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