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REVIEW ARTICLE
From the Laboratoire de Biologie des Cellules Souches
Somatiques Humaines, Centre National de la Recherche Scientifique,
Villejuif, France.
Hematopoiesis is a remarkable cell-renewal process that leads to
the continuous generation of large numbers of multiple mature cell
types, starting from a relatively small stem cell compartment. A highly
complex but efficient regulatory network is necessary to tightly
control this production and to maintain the hematopoietic tissue in
homeostasis. During the last 3 decades, constantly growing numbers of
molecules involved in this regulation have been identified. They
include soluble cytokines and growth factors, cell-cell interaction molecules, and extracellular matrix components, which provide a
multifunctional scaffolding specific for each tissue. The cloning of
numerous growth factors and their mass production have led to their
possible use for both fundamental research and clinical application.
(Blood. 2000;96:2022-2036) The regulation of hematopoiesis is a
complex process that has received much attention (for reviews see Moore
et al,1 1990; Metcalf,2 1993;
Ogawa,3 1993). Research continues to identify the various
components involved in this regulation (for review see Levesque et
al,4 1991). Many of the growth factors can now be cloned
for research and clinical purposes (for review see Simmons and
Haylock,5 1995).
Type At present, TGF- Latent and active forms
TGF-
Once synthesized and processed, TGF- Activation of latent TGF- Different mechanisms of activation are presented in Figure 1. Plasmin
has been shown to promote the activation of latent TGF-
Two families of serine/threonine kinase receptors form heteromeric complexes Among the several transmembrane or membrane-bound proteins known to interact with TGF- s, the type I and type II TGF-
receptors (TR-I or ALK, and TR-II) are directly involved in
signal transduction. TR-I and TR-II represent 2 families of
transmembrane serine/threonine kinase receptors of 53 to 65 kd47-49 and 80 to 95 kd,50 respectively, that
interact and form heterotetrameric complexes. The mechanism by which
signaling by these 2 receptors occurs is now well
established.51 TGF- first binds to TR-II, which is a
constitutively active kinase. TR-I is then recognized and recruited
into the TGF-/TR-II complex and phosphorylated by TR-II.
Phosphorylation allows TR-I to propagate the signal to downstream
intracellular substrates.
Because T Accessory receptors In addition to TR-I and TR-II, accessory TGF- receptors,
not necessarily required for signal transduction, can be expressed at
the surface of cells responsive to TGF- (for review see Piek et
al,52 1999). The type III TGF- receptor (TR-III or
glycan), a 300- to 400-kd membrane-anchored
proteoglycan,53,54 and the 180-kd glycoprotein endoglin
could function as regulators of ligand access to the signaling
receptors. Although the precise roles of endoglin and glycan are not
fully understood, some of their properties suggest distinct functions
for these 2 TGF- receptors. First, glycan is able to interact
with TGF-1, -2, and -3,55 whereas endoglin
interacts with TGF-1 and -3 but not efficiently with
TGF-2.56 Second, the role of glycan could be to
present TGF-s to TR-II and facilitate their
binding,57,58 whereas endoglin appears to diminish rather
than enhance TGF- responses in certain cell types.59
Third, endoglin and glycan possess a specific cell-distribution
pattern, which may confer the ability of different cell types to
respond differentially to TGF-1, -2, and -3. For example,
endoglin is coexpressed with TR-I and TR-II on vascular
endothelial cells60,61 and on hematopoietic cells including
macrophages,62 erythroid cell subsets,63 and
B-cell precursors,64 whereas these cells express little or
no glycan. Marrow stromal cells may express both endoglin and
glycan,65 whereas none of these TGF- receptors
appear to be present on the cell surface of hematopoietic
progenitors including early colony-forming units
(CFU)-granulocyte/erythrocyte/monocyte/megakaryocyte (GEMM),
CFU-granulocyte/monocyte (GM), and burst-forming units-erythrocyte (BFU-E).63
Other cell-surface receptors have been identified for their ability to
bind TGF- The Smad intracellular proteins The intracellular TGF- signaling pathway involves the Smad
protein family as substrates for the signaling receptors (for review
see Massagué,67 1998; Piek et al,52
1999). This network involves the cooperation among 3 subclasses of Smad
proteins, which can be distinguished by distinct functions in TGF-
signal transduction. Briefly, a first group of Smads called
"receptor-activated"67 or
"receptor-regulated"52 Smads (R-Smads) are directly
phosphorylated by activated TR-I. Upon phosphorylation, R-Smads
interact with members of a second subclass of Smads called
"common-partner Smads" or Co-Smads, with which they form
heterodimeric complexes. R-Smad/Co-Smad complexes are translocated to
the nucleus, where they associate with DNA-binding partners and then
regulate the transcriptional response of the target genes. A third
subclass of Smads called "antagonistic"67 or
"inhibitory"52 Smads (Anti-Smads) prevents the
interaction between R-Smads and Co-Smads and participates in negative
feedback to repress TGF- responses. In the case of signal
transduction by TGF- in mammalian cells, R-Smads include Smad2 and
Smad3,68,69 Co-Smads include Smad4,69,70 and
Anti-Smads include Smad6 and Smad7.71-73 Smad5, otherwise
described as an R-Smad and involved in signal transduction by bone
morphogenetic proteins (BMPs),74 has been demonstrated to
mediate the inhibitory effect of TGF- on human hematopoietic
stem/progenitor cells.75 The specificity of the cellular
response depends on interactions between these different
possible partners.
Studies of hematopoietic pathologies involving TGF- Inactivation of the TGF- signal transduction pathway may represent a possible mechanism by which some early hematopoietic progenitors, which are normally quiescent, escape from cell-cycling inhibition. Abnormalities in the
expression of TGF- receptors have been described in proliferative syndromes including both early myeloid76,77 and lymphocytic leukemia.78,79 In these pathologies, a selective advantage is given to the tumor cells by the loss of TR-I or TR-II
expression and by the fact that these cells continue to produce
TGF-1 to inhibit normal cell proliferation. Active TGF- present
in the bone marrow microenvironment and autocrine/paracrine TGF-1
secreted by normal and leukemic hematopoietic cells are able to exert a negative control on the growth of normal progenitors, but not on
leukemic cells, which have overcome TGF- regulatory signals. A loss
of sensitivity to the growth-inhibitory effect of TGF- due to an
inactivation of TR-II has also been described in the case of human
cutaneous T-cell lymphoma cells.80-82
A mutational analysis of the gene coding for the TGF- Pathologic overproduction of TGF- produced by bone
marrow stromal cells and hematopoietic cells should be adequate to
maintain homeostasis of the stem/progenitor cell compartment. In
pathologic situations, excessive production of TGF- by stromal cells
has been correlated with a failure of early hematopoietic progenitors
in the marrow. This situation has been described in the case of human
chronic idiopathic neutropenia, in which a drastic reduction in
CD34+ progenitor cell frequency is observed.87
The same phenomenon has been described for B-cell lymphocytic leukemia.
In this case, the pathogenesis is due to the proliferation of leukemic
cells, but also to an increased inhibition of normal progenitor cell growth, in response to excessive amounts of TGF-1 secreted by bone
marrow stromal cells.88
An abnormally elevated production of TGF- Vascular pathologies involving TGF- receptor have also been
correlated with the genetic diseases called hereditary hemorrhagic telangiectasia (HHT). These syndromes concern mainly endothelial cells
and are characterized by arteriovenous malformations and recurrent
hemorrhage. HHT syndromes were first found to be caused by mutations in
the endoglin gene95 but have also been correlated with
mutations in the TR-I
gene,96 suggesting that endoglin and TR-I act through a
common pathway to control blood vessel development and repair.
TGF- TGF- signaling cascade participates in malignant transformation of early hematopoietic cells, which then escape from
negative cell-cycle controls. It is interesting to note that the same
phenomenon has been described in cancers affecting various types of
nonhematopoietic somatic cells, which suggests that TGF- may act as
a cell-cycle inhibitor in several nonhematopoietic somatic tissues in
vivo. Indeed, although they probably do not represent the entire cause
of the pathology, mutations or genetic defects resulting in a lack of
TR-I or TR-II function are associated with the acquisition of a
transformed phenotype in several types of murine and human cancers,
including colon cancers,98,99 gastric
cancers,100,101 prostate cancers,102
pancreatic cancers,103 thyroid tumors,104
hepatic tumors,105,106 retinoblastoma,107,108 and lung adenocarcinoma.109 Moreover, the importance of
TGF- signaling for the control of normal somatic cell proliferation has been demonstrated in skin keratinocytes,110,111 cells
of the mammary gland, lung,112 and exocrine
pancreas113 with the use of transgenic mice expressing a
dominant-negative mutant TR-II (for review see Letterio and
Bottinger,114 1998).
In addition, elements of the TGF-
The role of TGF- TGF- to
affect hematopoietic stem/progenitor cell cycling. TGF-1 has been
shown to delay hematologic recovery after a sublethal injection of
5-FU.121 Moreover, both the TGF-1 and -2 isoforms
were able to protect hematopoietic stem/progenitor cells from a
treatment by a high dose of 5-FU,122 which demonstrates
the ability of these molecules to exert a negative control on the cell
cycle of primitive murine hematopoietic cells in vivo. It is important
to note that this effect was reversible,121,122 which
suggests that TGF- is not an inducer of cell death for primitive
stem/progenitor cells in vivo. This point will be discussed more
extensively later.
In vivo administration of TGF- in mice has also been performed
to study its specific effects on early and late progenitors and on the
different hematopoietic lineages. One approach, which was to test in
vitro the clonogenic capacity of hematopoietic progenitors after the
local administration of TGF-1 into the femur of mice, revealed a
preferential growth-inhibitory effect of this factor on the earlier
progenitors.123 A second approach was to perform
histologic analyses of hematopoietic tissues from mice treated with
TGF-1. Such studies revealed an inhibition of erythropoiesis and
thrombopoiesis in TGF-1-treated mice,124,125 whereas
granulopoiesis was stimulated.124-126 Although some of
these effects may be directly mediated, the possibility that
administration of exogenous TGF- in vivo may deregulate the
production of other factors involved in the control of hematopoiesis
should be taken into account. For example, an increased production of
tumor necrosis factor (TNF)- has been observed after the
administration of TGF- in mice.127
Hematopoiesis in knockout mice An opposing strategy has been to study in vivo the development of the hematopoietic tissue in the absence of endogenous TGF-, or in a
context in which the cell responsiveness to TGF- is abrogated. For
this purpose, a variety of knockout mice have been generated, in which
a targeted disruption of genes encoding a TGF- isoform or another
element of the TGF- signaling cascade has been performed. Homozygous
TGF-1 knockout mice have a
50% intrauterine death rate because of severe developmental
retardation. Defective hematopoiesis, resulting in a reduced number of
erythroid cells128 as well as a lack of Langerhans
dendritic cells,129 has been correlated with the absence
of TGF-1. However, TGF-1
knockout mice also present defects in liver development130
and bone formation,131 as well as many other
dysregulations including autoimmune manifestations.132,133 The phenotype of TR-II
knockout mice has been reported to be indistinguishable from that of
TGF-1 knockout
mice.134 Mice lacking endoglin show defective
angiogenesis,135 providing a good animal model of
HHT.136 TGF-3
knockout mice show abnormal lung and craniofacial development due to
altered epidermal-mesenchymal interactions,137 but these
mice do not provide clear information concerning the role of this gene
in the development of hematopoietic tissue. Knockout mice for the
TGF-2 gene exhibit a wide
range of developmental defects that do not overlap with those of the other TGF- knockout
phenotypes.138 Concerning the Smad genes, Smad3 knockout mice demonstrate defects in immune
function,139 whereas Smad4 and Smad5
knockout mice have multiple embryonic and extraembryonic
defects.140,141
Human and murine hematopoietic stem/progenitor cells are
usually in a quiescent or slow cycling state in
adults.142,143 As suggested by in vivo studies, TGF- TGF- added to clonal cultures of hematopoietic progenitors. The first TGF- isoform, TGF-1, has been shown to inhibit colony formation by early murine144-146 and human hematopoietic
progenitors in semisolid media,147-149 but not that of
late progenitors.145,147-149
In these studies, the effects of TGF- An alternative approach has been to use blocking antibodies or
antisense oligonucleotides to neutralize TGF- Since the first studies on TGF- Preferential growth inhibition of the most primitive human
hematopoietic cells has also been reported in studies in which the
effects of anti-TGF- The second isoform, TGF- TGF- Studies performed on adherent bone marrow primary stromal cells or cell
lines have shown that these cells can produce a variety of growth
factors, including cytokines such as G-CSF; GM-CSF162,163; IL-1 The term "long-term culture initiating cell" (LTC-IC) has been
assigned to a subpopulation of primitive human hematopoietic stem/progenitor cells that possess the potential to sustain continuous production of progenitors for at least 8 weeks in the presence of
stroma.161 Anti-TGF- Similar observations have been reported for murine hematopoietic
stem/progenitor cells cultured according to the Dexter method. Dexter-type culture systems consist of total marrow cultures in which
an expansion of primitive hematopoietic stem/progenitor cells is
maintained for several months because of the presence of a bone
marrow-derived adherent layer consisting of different types of
nonhematopoietic accessory cells including adipocytes.169 The addition of antibodies neutralizing the biologic activity of
TGF- These stroma-supported in vitro culture systems have provided important
information concerning the role of TGF- Remarks All of these in vitro studies converge to suggest that TGF-
inhibits preferentially the cell cycling of the most primitive hematopoietic cells. These results have also been reproduced in an in
vivo model. Indeed, nonobese diabetic/severe combined immunodeficient mice have been transplanted with human bone marrow and umbilical cord
blood cells and injected with TGF-1 at 6 weeks after
transplantation. Analysis of the specific responses of different
progenitor cell types has revealed that TGF-1 is active on primitive
progenitor cell populations, including LTC-IC and HPP-colony-forming
cells, but not on the more mature cells.171
It should be pointed out that differences in the responsiveness to
TGF-
TGF- to modulate the expression of cytokine
receptors has been observed both in transformed cell lines and in
normal hematopoietic progenitors. In murine progenitor cell lines,
TGF- has been shown to down-modulate the expression of the receptors
for IL-1,173 IL-3, G-CSF, and GM-CSF.174 In
normal hematopoietic bone marrow cells, similar observations were made in humans for the IL-1 receptor173 and in mice for the
IL-1, IL-3, and the M-CSF receptors, but not for the GM-CSF receptor which, on the contrary, is up-modulated by TGF- on murine progenitor cells.175,176 G-CSF receptor expression was not
affected.176 These effects appear to be isoform dependent.
For example, TGF-3 may be a more potent inhibitor of IL-3 receptor
expression than TGF-1, whereas TGF-3 is less efficient than
TGF-1 in stimulating the expression of the GM-CSF
receptor.176
More recently, TGF- The HPP-Q working model The concept of the high-proliferative-potential quiescent cell (HPP-Q) has been introduced to refer to a primitive subpopulation of human hematopoietic stem/progenitor cells that are highly sensitive to growth inhibition by TGF-1.181 TGF-1 maintains
these cells in a quiescent or slow cycling state by down-modulating
various cytokine receptors, preventing them from responding rapidly to mitogenic stimulation (Figure 2). In the
in vitro HPP-Q assay, which can be performed both in semisolid
conditions and in single-cell liquid cultures,150,181
the use of antisense oligonucleotides or anti-TGF-1 blocking
antibodies allows these primitive cells to escape from cell-cycle
inhibition. A short treatment with anti-TGF-1 is sufficient to
activate HPP-Q cells and render them competent and responsive to
cytokines (Figure 2). Indeed, similar effects were obtained when cells
were pretreated for only 6 to 12 hours before plating and when
anti-TGF-1 was maintained or added repeatedly throughout the
culture period (Hatzfeld A et al, unpublished results).
The HPP-Q population presents at least 3 characteristics of a primitive stem/progenitor cell compartment: (1) HPP-Q cells possess a high proliferative potential, as they are able to generate, within 18 days, clones containing more than 105 cells when cultured in a liquid medium in single-cell conditions; (2) they give rise to multilineage hematopoietic clones or colonies when cultured in the presence of the appropriate cytokine combination; and (3) they are in a quiescent or slow cycling state in spite of their high proliferative potential. A fourth characteristic of the HPP-Q cell population is under study. It concerns the ability of HPP-Q cells to promote long-term engraftment. One main interest of this working model is the possibility of further phenotyping HPP-Q stem/progenitor cells on the basis of cytokine receptor expression. These cells express low levels of various cytokine receptors such as KIT, FLT3, IL-6R, and MPL. This renders possible the sorting of cell subpopulations enriched in HPP-Q stem/progenitor cells. The long-term engraftment capacity of CD34+/ KITlow/ FLT3low/ IL-6Rlow/ MPLlow cells should be studied in xenograft animal models such as preimmune sheep fetuses.185 Up to now, in this sheep model, the CD34+/ KITlow population, which includes HPP-Q cells, has been reported to contain the marrow-engrafting stem/progenitor cells. This was not the case for KIThigh and KITneg cells.186
The identification of growth inhibitors able to control the
proliferation of leukemic cells is of particular importance in the
development of therapeutic approaches. As stated earlier, the
acquisition of resistance to growth inhibition by TGF- The relations between TGF-
TGF- is one of the key regulators of erythropoiesis because it
is involved in the control of both early and later stages of erythroid
progenitor cell development (Figure 3).
The first isoform, TGF-1, has been identified as a cell-cycle
inhibitor for early human and mouse BFU-E, but not for later erythroid
progenitors, which are poorly affected by its growth-inhibitory
effect.150,154,155,205 This negative regulation occurs in
part through an autocrine negative-control loop.150 It has
been reported that TGF-2 and TGF-3 could also inhibit the
development of human BFU-E,149 but the effects of these 2 isoforms on erythropoiesis have not been investigated in
detail.
In contrast, TGF- In addition to its role in the control of erythroid progenitor cell
proliferation, TGF- As already described, TGF- Another key regulator of erythropoiesis is Epo. In addition to being
the principal factor promoting the terminal differentiation of
erythrocytes, this cytokine is able to stimulate earlier stages of
erythropoiesis. Indeed, Epo is well known to stimulate the growth and
development of CFU-E, and has been shown to sustain the proliferation
of some BFU-E, but only if anti-TGF- Other reports provide convincing evidence that TGF- Bidirectional effects of TGF- on myelopoiesis have been described in vitro (Figure 3). Inhibitory effects were mainly observed
on the earlier bipotent myeloid progenitors, whereas cells in later
stages were either slightly inhibited or even stimulated, depending on
the other factors present. TGF-1 added to a semisolid medium
containing IL-3, IL-6, IL-11, Epo, SF, GM-CSF, and G-CSF has been found
to inhibit the growth of early human HPP-GM, but not that of late CFU-G
and CFU-M.154 In contrast, when the TGF-1 regulatory
effects were studied in the presence of individual cytokines, clear
stimulating effects were observed on the middle and late stages of
myeloid cell development. As an example, in culture media containing
only GM-CSF and TGF-1, these 2 factors were found to synergize and
then promote the development of a population of human mid-stage CFU-GM
(day-7 CFU-GM), whereas earlier CFU-GM (day-14 CFU-GM) were not
stimulated.149
The effects of TGF- In contrast to what has been observed for many cytokine receptors
controlling the cell cycling of hematopoietic stem/progenitor cells,
TGF- Control of early and late megakaryopoiesis by TGF- Early megakaryocytic progenitors first enter into a proliferating
state when stimulated by appropriate growth factors. For instance,
IL-3, IL-6, IL-11, SF, and TPO have been identified as potent
"early-acting" Mk-stimulating factors.226-230 In
contrast, several studies have shown TGF- TGF- TGF- We have described the ability of TGF- TGF- on lymphoid cell lineages would
require a specific review. Here we will just mention the role of
TGF- in the regulation of the development of cells of the immune
system by introducing the case of dendritic cells (DCs) (Figure 3).
TGF- contributes to the generation of DCs, which correspond to a
particular population of leukocytes specialized in antigen presentation
for T-cell responses. DCs can be obtained in vitro from human
CD34+ cells,197,245 murine lineage-negative
(Lin )KIT+ cells,246 human
monocytes,247-249 and from their
precursors.250
In vitro studies have demonstrated that the growth-factor requirement
for the development of DCs includes TGF- Generation of human and mouse DCs in response to TGF-
Efficient retroviral-mediated gene transfer into stem/progenitor
cells released from quiescence by anti-TGF- 1 produced by hematopoietic progenitors is partly
responsible for their maintenance in a quiescent or slow cycling
state,150,151 the use of anti-TGF-1 blocking
antibodies to neutralize the bioactivity of endogenous TGF-1 during
the retroviral transfection procedure was attempted to increase gene
transfer into primitive stem/progenitor cells. This strategy has been
tested with success on hematopoietic cells of several origins,
including human umbilical cord blood,254 bone
marrow,255 peripheral blood,256 and murine
bone marrow.257 The efficiency of this method was shown to
be improved by the coupled use of anti-TGF-1 blocking antibodies
with antisense oligonucleotides against the cyclin-dependent kinase
inhibitor (CDKI) p27kip1.255 This
approach could be extended to other effectors involved in the negative
regulation of hematopoietic stem/progenitor cell cycling by TGF-1,
such as pRb150 or the CDKI
p21cip1.258
Moreover, it has been observed that CD34+ cells produce
TGF- In vitro amplification of stem/progenitor cells: key role
of TGF- TGF-
The pleiotropic effects of TGF- Despite the considerable numbers of studies performed to understand the
complex regulatory role of TGF- In this review, we have focused on studies performed on TGF- Signal transduction by the members of the TGF- In conclusion, the development of therapeutic agents to correct, in
vivo, dysfunctions of the TGF-
We are indebted to Dr Mary Osborne for her critical reading of the manuscript.
Submitted February 3, 2000; accepted April 10, 2000.
Supported by European Contract no. BIO4-CT96-0646, the Centre National de la Recherche Scientifique (CNRS), and the Association pour la Recherche sur le Cancer (ARC).
The publication costs of this article were defrayed in part by page charge payment. Therefore, and solely to indicate this fact, this article is hereby marked "advertisement" in accordance with 18 U.S.C. section 1734.
Reprints: Jacques A. Hatzfeld, Laboratoire de Biologie des Cellules Souches Somatiques Humaines, UPR 1983, Centre National de la Recherche Scientifique, IFC1, 7, rue Guy Môquet, 94800, Villejuif, France; e-mail: hatzfeld{at}infobiogen.fr.
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S. Charrier, A. Michaud, S. Badaoui, S. Giroux, E. Ezan, F. Sainteny, P. Corvol, and W. Vainchenker Inhibition of angiotensin I-converting enzyme induces radioprotection by preserving murine hematopoietic short-term reconstituting cells Blood, August 15, 2004; 104(4): 978 - 985. [Abstract] [Full Text] [PDF]
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I. Dybedal, L. Yang, D. Bryder, I. Aastrand-Grundstrom, K. Leandersson, and S. E. W. Jacobsen Human reconstituting hematopoietic stem cells up-regulate Fas expression upon active cell cycling but remain resistant to Fas-induced suppression Blood, July 1, 2003; 102(1): 118 - 126. [Abstract] [Full Text] [PDF]
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D. Bryder, V. Ramsfjell, I. Dybedal, K. Theilgaard-Monch, C.-M. Hogerkorp, J. Adolfsson, O. J. Borge, and S. E. W. Jacobsen Self-Renewal of Multipotent Long-Term Repopulating Hematopoietic Stem Cells Is Negatively Regulated by FAS and Tumor Necrosis Factor Receptor Activation J. Exp. Med., October 1, 2001; 194(7): 941 - 952. [Abstract] [Full Text] [PDF]
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| Copyright © 2000 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
: pleiotropic role in the
regulation of hematopoiesis
Top
Abstract
Introduction
s
many of which
could not be cited here because of space limitations