Effects of fibroblast growth factor-4 (k-FGF) on long-term cultures of human bone marrow cells

Quito, Francis L.; Beh, Jane; Bashayan, Omar; Basilico, Claudio; Basch, Ross S.

doi:10.1182/blood.v87.4.1282.bloodjournal8741282

Cited by 37 publications

(20 citation statements)

References 31 publications

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“…Several groups have investigated the effects of growth factors on marrow stromal cells. [39][40][41][42][43][44][45][46][47] Of note, BMSCs are a heterogeneous population of cells that reside in the postnatal bone marrow cavity in tight contact with Gronthos et al have demonstrated that, in the absence of serum, growth factors are required for the prolifera-and supporting the hematopoietic compartment. [25][26][27] They are clonogenic and are also referred to as colony-forming tion of BMSC in culture.…”

Section: Bmsc Fatementioning

confidence: 99%

Microenvironment and stem properties of bone marrow‐derived mesenchymal cells

Bianchi

Muraglia²,

Daga

et al. 2001

Wound Repair Regeneration

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Adult stem cells are self-renewing, pluripotent, and able to repopulate the tissue in which they reside. Cells endowed with these properties have been isolated from several tissues and an increasing number of reports provide evidence of their ability, following transplantation, to engraft host tissues other than those of their origin. In this setting, interest in the well-documented capacity of bone marrow stromal cells to undergo multilineage differentiation is growing. Neural and cardiomyogenic lineages have recently been proposed as additional differentiative pathways of these cells. However, culture conditions and inductive molecules can alter the behavior of bone marrow stromal cells and the microenvironment is critical for proper in vivo delivery. The maintenance of their stem properties and the possibility of reprogramming their commitment is a field of primary interest given the potential use of these cells in regenerative medicine. We discuss here how the microenvironmental cues, and the growth factors that physiologically govern commitment and subsequent differentiation, influence the properties of bone marrow stromal cells and modulate their engraftment into host tissues.

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Section: Bmsc Fatementioning

confidence: 99%

Microenvironment and stem properties of bone marrow‐derived mesenchymal cells

Bianchi

Muraglia²,

Daga

et al. 2001

Wound Repair Regeneration

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“…In cultures of normal long term bone marrow cells, TGF-b has been found to be a potent inhibitor of progenitor cell cycling and the addition of neutralising antibodies to TGF-b increases the percentage of progenitor cells in S phase (Eaves et al, 1991). In contrast, FGFs have been noted to signi®cantly enhance the progenitor content of long term bone marrow cultures Quito et al, 1996). These results indicate that one of the functions of bFGF in the hematopoietic environment may be to oppose or counterbalance the effects of TGF-b on hematopoietic cells.…”

Section: Discussionmentioning

confidence: 99%

“…Receptors for FGFs have been found on K562 cells (Allouche, 1995;Liuzzo and Moscatelli, 1996) and on CD34 hematopoietic progenitor cells (Berardi et al, 1995;Le Bousse-Kerdil Á es et al, 1996;Testa et al, 1996;Burger et al, 1998Burger et al, , 1999 and direct effects of bFGF have been shown on progenitor cell proliferation (Gabbianelli et al, 1990;Bruno et al, 1993;Gabrilove et al, 1994;Allouche, 1995;Berardi et al, 1995). These direct effects are signi®cantly less than those noted when bFGF is added to stromal based hematopoietic cultures Quito et al, 1996). It is possible that the effects of bFGF in stromal based cultures are signi®-cantly greater than direct effects on isolated progenitor cells, as one of the important functions of bFGF may be to oppose TGF-b which is produced in signi®cant quantities by bone marrow stromal cells (Eaves et al, 1991;Coetzee et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

“…bFGF is also found in megakaryocytes (Brunner et al, 1993), T cells (Peoples et al, 1995) and leukemic cells (Allouche, 1995;Menzel et al, 1996). It synergises with other cytokines to stimulate the growth of puri®ed hematopoietic progenitor cells and stimulates myelopoiesis in human longterm bone marrow cultures (Gabbianelli et al, 1990;Wilson et al, 1991;Bruno et al, 1993;Gabrilove et al, 1994;Allouche, 1995;Quito et al, 1996). It stimulates the growth of a primitive erythroid cell line and inhibits its ability to undergo erythroid differentiation (Yuen et al, 1998).…”

mentioning

confidence: 99%

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Basic fibroblast growth factor modulates the expression of glycophorin A and c‐kit and inhibits erythroid differentiation in K562 cells

Burger¹,

Lukey²,

Coetzee³

et al. 2001

Journal Cellular Physiology

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Basic fibroblast growth factor (bFGF) is produced by bone marrow stromal cells as well as by normal and leukemic hematopoietic cells. In this study, we examine the direct effects of bFGF on erythroid differentiation in K562 cells in order to determine whether bFGF can promote the expression of a primitive phenotype. Low levels of bFGF inhibited erythroid differentiation as evidenced by decreased expression of glycophorin A and increased expression of c-kit. bFGF also increased both the numbers and the sizes of colonies of K562 cells in soft agar assays. The addition of TGF-beta to these cells induced erythroid differentiation which resulted in an increase in glycophorin A and a decrease in c-kit. The simultaneous addition of bFGF and TGF-beta to K562 cells prevented both the TGF-beta-mediated increase in glycophorin A expression and the decrease in c-kit expression associated with erythroid differentiation. bFGF antagonised the TGF-beta-mediated promotion of erythroid differentiation in K562 cells in a dose dependent manner and these two cytokines counteracted each other on an approximately molar basis. These results indicate that bFGF alone increases expression of c-kit and promotes a primitive phenotype in K562 cells. In addition, bFGF counteracts the effects of differentiation-inducing cytokines, such as TGF-beta, on hematopoietic cells. It is therefore possible that enhanced production of bFGF by leukemic cells could contribute to their neoplastic phenotype by opposing the effects of negative regulators or cytokines that induce differentiation.

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“…The growth factor requirement for the in vitro expansion of BMSCs has been investigated by several groups [28][29][30][31][32][33][34]. Gronthos and Simmons demonstrated that, in the absence of serum, growth factors are necessary for the proliferation of BMSCs in culture [29].…”

Section: Osteogenic Progenitors From Bmmentioning

confidence: 99%

Cell Therapy for Bone Disease: A Review of Current Status

et al. 2003

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Bone marrow is a reservoir of pluripotent stem/progenitor cells for mesenchymal tissues. Upon in vitro expansion, in vivo bone-forming efficiency of bone marrow stromal cells (BMSCs) is dramatically lower in comparison with fresh bone marrow, and their in vitro multidifferentiation potentials are gradually lost. Nevertheless, when BMSCs are isolated and expanded in the presence of fibroblast growth factor 2, the percentage of cells able to differentiate into the osteogenic, chondrogenic, and adipogenic lineages is greater. Osteogenic progenitors are not exclusive to skeletal tissues. We could also think of cells in different adult tissues as potentially capable of following an osteochondrogenic differentiation pathway, but, under normal physiological conditions, they are inhibited in this process by the environment and/or the adjacent cell populations. When, for some reason such as pathology, the environment changes dramatically and the inhibiting condition is removed, these cells could become osteoblasts. Bone is repaired via local delivery of cells within a scaffold. Bone formation was first assessed in small animal models. Large animal models were successively developed to prove the feasibility of the tissue engineering approach in a model closer to a real clinical situation. Eventually, pilot clinical studies were performed. Extremely appealing is the possibility of using mesenchymal progenitors in the therapy of genetic bone diseases via systemic infusion. There is experimental evidence to suggest that mesenchymal progenitors delivered by this route engraft with a very low efficiency and do not produce relevant and durable clinical effects. Under some conditions, where the local microenvironment is either altered (i.e., injury) or under important remodeling processes (i.e., fetal growth), engraftment of stem and progenitor cells seems to be enhanced. A better understanding of their engraftment mechanisms will, hopefully, extend the field of therapeutic applications of mesenchymal progenitors.

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Effects of fibroblast growth factor-4 (k-FGF) on long-term cultures of human bone marrow cells

Cited by 37 publications

References 31 publications

Microenvironment and stem properties of bone marrow‐derived mesenchymal cells

Microenvironment and stem properties of bone marrow‐derived mesenchymal cells

Basic fibroblast growth factor modulates the expression of glycophorin A and c‐kit and inhibits erythroid differentiation in K562 cells

Cell Therapy for Bone Disease: A Review of Current Status

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