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Tumor necrosis factor (TNF) is a physiologic regulator of hematopoietic
progenitor cells: increase of early hematopoietic progenitor cells in TNF
receptor p55-deficient mice in vivo and potent inhibition of progenitor
cell proliferation by TNF alpha in vitro
Y Zhang, A Harada, H Bluethmann, JB Wang, S Nakao, N Mukaida and K Matsushima
Department of Pharmacology, School of Medicine, Kanazawa University, Japan.
Murine bone marrow cells with lineage phenotypes (Lin)-Sca-1+c-kit+ and
Lin-Sca-1-c-kit+ cells represent primitive hematopoietic stem cells (HSCs)
and committed hematopoietic progenitor cells, respectively. The number of
Lin-Sca-1+c-kit+ HSCs in bone marrow was significantly increased in tumor
necrosis factor (TNF) receptor p55-deficient (TNF- R55-1-) mice compared
with the TNF-R55+/+ wild-type mice without a marked change in bone marrow
cellularity. In both the methylcellulose culture and a single-cell
proliferation assay, mouse TNF alpha (mTNF alpha) inhibited in vitro the
proliferation of wild-type mouse-derived Lin-Sca-1+c-kit+ cells in response
to a combination of multiple growth factors. The same is true for that of
Lin-Sca-1+c-kit+ cells stimulated with granulocyte colony-stimulating
factor (G-CSF) plus stem cell factor (SCF). Moreover, mTNF alpha
significantly arrested the entry into S-phase from G0/G1 phase of
Lin-Sca-1+c-kit+ cells stimulated with multiple growth factors and
Lin-Sca-1-c-kit+ cells stimulated with G- CSF plus SCF. In contrast, mTNF
alpha failed to affect the growth and cell cycle progression of
Lin-Sca-1+c-kit+ cells and Lin-Sca-1-c-kit+ cells that were obtained from
TNF-R55-deficient mice. These data suggest that TNF may be an important
physiologic regulator of hematopoiesis and that TNF-R55 may be essentially
involved in TNF- mediated inhibition of the growth of both primitive stem
and more committed progenitor cells.
Volume 86,
Issue 8,
pp. 2930-2937,
10/15/1995
Copyright © 1995 by The American Society of Hematology
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