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Distinct and overlapping direct effects of macrophage inflammatory
protein-1 alpha and transforming growth factor beta on hematopoietic
progenitor/stem cell growth
JR Keller, SH Bartelmez, E Sitnicka, FW Ruscetti, M Ortiz, JM Gooya and SE Jacobsen
Biological Carcinogenesis and Development Program, Program Resources,
Inc/DynCorp, National Cancer Institute (NCI)-Frederick Cancer Research and
Development Center, MD 21702-1201.
Both transforming growth factor beta (TGF beta) and macrophage inflammatory
protein 1 alpha (MIP-1 alpha) have been shown to be multifunctional
regulators of hematopoiesis that can either inhibit or enhance the growth
of hematopoietic progenitor cells (HPC). We report here the spectrum of
activities of these two cytokines on different hematopoietic progenitor and
stem cell populations, and whether these effects are direct or indirect.
MIP-1 alpha enhances interleukin-3 (IL- 3)/and granulocyte-macrophage
colony-stimulating factor (GM- CSF)/induced colony formation of normal bone
marrow progenitor cells (BMC) and lineage-negative (Lin-) progenitors, but
has no effect on G- CSF or CSF-1/induced colony formation. Similarly, TGF
beta enhances GM- CSF/induced colony formation of normal BMC and Lin-
progenitors. In contrast, TGF beta inhibits IL-3/ and CSF-1/induced colony
formation of Lin- progenitors. The effects of MIP-1 alpha and TGF beta on
the growth of Lin- progenitors were direct and correlate with colony
formation in soft agar. Separation of the Lin- cells into Thy-1 and Thy-1lo
subsets showed that the growth of Thy-1lo Lin- cells is directly inhibited
by MIP-1 alpha and TGF beta regardless of the cytokine used to stimulate
growth (IL-3), GM-CSF, or CSF-1). In contrast, two other stem cell
populations (0% to 15% Hoechst 33342/Rhodamine 123 [Ho/Rh123] and Lin-
Sca-1+ cells) were markedly inhibited by TGF beta and unaffected by MIP- 1
alpha. Furthermore, MIP-1 alpha has no effect on high proliferative
potential colony-forming cells 1 or 2 (HPP-CFC/1 or /2) colony formation in
vitro, whereas TGF beta inhibits both HPP-CFC/1 and HPP- CFC/2. Thus, MIP-1
alpha and TGF beta are direct bidirectional regulators of HPC growth, whose
effects are dependent on other growth factors present as well as the
maturational state of the HPC assayed. The spectrum of their inhibitory and
enhancing activities shows overlapping yet distinct effects.
Volume 84,
Issue 7,
pp. 2175-2181,
10/01/1994
Copyright © 1994 by The American Society of Hematology
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