Use of Neopterin as a Bone Marrow Hematopoietic and Stromal Cell Growth Factor in Tissue-Engineered Devices

2007 ◽  
pp. 115-121
Author(s):  
E. Zvetkova ◽  
Y. Gluhcheva ◽  
D. Fuchs
Keyword(s):  
Bone Marrow ◽  
Growth Factor ◽  
Cell Growth ◽  
Stromal Cell

scholarly journals Mast cell growth factor (c-kit ligand) supports the growth of human multipotential progenitor cells with a high replating potential

Blood ◽  
1991 ◽  
Vol 78 (9) ◽  
pp. 2216-2221 ◽  
Author(s):  
CE Carow ◽  
G Hangoc ◽  
SH Cooper ◽  
DE Williams ◽  
HE Broxmeyer
Keyword(s):  
Bone Marrow ◽  
Mast Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
Cord Blood ◽  
Primary Cultures ◽  
Human Umbilical Cord Blood ◽  
Human Umbilical Cord ◽  
Factor C ◽  
Mast Cell Growth Factor

Abstract The replating capability of human multipotential (colony-forming unit- granulocyte-erythrocyte-macrophage-megakaryocyte [CFU-GEMM]) and erythroid (burst-forming unit-erythroid [BFU-E]) progenitors was assessed in vitro as a potential measure of self-renewal using purified, recombinant (r) human (hu) or murine (mu) mast cell growth factor (MGF), a ligand for the c-kit proto-oncogene receptor. Primary cultures of human umbilical cord blood or adult human bone marrow cells were initiated in methylcellulose with erythropoietin (Epo) alone or in combination with rhu interleukin-3 (IL-3) or MGF. Individual day 14 to 18 CFU-GEMM or BFU-E colonies were removed from primary cultures and reseeded into secondary methylcellulose cultures containing a combination of Epo, MGF, and rhu granulocyte-macrophage colony- stimulating factor (GM-CSF). The data showed a high replating efficiency of cord blood and bone marrow CFU-GEMM in response to Epo + MGF in terms of the percentage of colonies that could be replated and the number of secondary colonies formed per replated primary colony. The average number of hematopoietic colonies and clusters apparent from replated cultures of cord blood or bone marrow CFU-GEMM stimulated by Epo + MGF was greater than with Epo + rhuIL-3 or Epo alone. Replated cord blood CFU-GEMM gave rise to CFU-GEMM, BFU-E, and GM colony-forming units (CFU-GM) in secondary cultures. Replated bone marrow CFU-GEMM gave rise mainly to CFU-GM in secondary cultures. A more limited capacity for replating of cord blood and bone marrow BFU-E was observed. These studies show that CFU-GEMM responding to MGF have an enhanced replating potential, which may be promoted by MGF. These studies also support the concept that MGF acts on more primitive progenitors than IL-3.

Evaluation of human bone marrow stromal cell growth on biodegradable polymer/Bioglass® composites

2006 ◽  
Vol 342 (4) ◽  
pp. 1098-1107 ◽  
Author(s):  
Xuebin B. Yang ◽  
Derek Webb ◽  
Jonny Blaker ◽  
Aldo R. Boccaccini ◽  
Veronique Maquet ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Growth ◽  
Biodegradable Polymer ◽  
Stromal Cell ◽  
Bone Marrow Stromal Cell ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Marrow Stromal Cell

scholarly journals Transforming growth factor-β1 modulates responses of CD34+ cord blood cells to stromal cell-derived factor-1/CXCL12

Blood ◽  
2005 ◽  
Vol 106 (2) ◽  
pp. 485-493 ◽  
Author(s):  
Sunanda Basu ◽  
Hal E. Broxmeyer
Keyword(s):  
Bone Marrow ◽  
Growth Factor ◽  
Cord Blood ◽  
Progenitor Cells ◽  
Stromal Cell ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Cd34 Cells ◽  
Stromal Cell Derived Factor ◽  
Tgf Β1

Abstract Disruption of stromal cell-derived factor-1 (SDF-1/CXCL12 [CXC chemokine ligand 12]) interaction leads to mobilization of stem/progenitor cells from bone marrow to circulation. However, prolonged exposure of CD34+ cells to SDF-1 desensitizes them to SDF-1. So how do cells remain responsive to SDF-1 in vivo when they are continuously exposed to SDF-1? We hypothesized that one or more mechanisms mediated by cytokines exist that could modulate SDF-1 responsiveness of CD34+ cells and the desensitization process. We considered transforming growth factor-β1 (TGF-β1) a possible candidate, since TGF-β1 has effects on CD34+ cells and is produced by stromal cells, which provide niches for maintenance and proliferation of stem/progenitor cells. TGF-β1 significantly restored SDF-1–induced chemotaxis and sustained adhesion responses in cord blood CD34+ cells preexposed to SDF-1. Effects of TGF-β1 were dependent on the dose and duration of TGF-β1 pretreatment. Phosphorylation of extracellular signal-regulated kinase 1 (Erk1)/Erk2 was implicated in TGF-β1 modulation of migratory and adhesion responses to SDF-1. Our results indicate that low levels of TGF-β1 can modulate SDF-1 responsiveness of CD34+ cells and thus may facilitate SDF-1–mediated retention and nurturing of stem/progenitor cells in bone marrow.

Ischemic rat brain extracts induce human marrow stromal cell growth factor production

2002 ◽  
Vol 22 (4) ◽  
pp. 275-279 ◽  
Author(s):  
Xiaoguang Chen ◽  
Yi Li ◽  
Lei Wang ◽  
Mark Katakowski ◽  
Lijie Zhang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Rat Brain ◽  
Stromal Cell ◽  
Marrow Stromal Cell ◽  
Factor Production ◽  
Brain Extracts ◽  
Growth Factor Production

scholarly journals T-cell growth factor P40 promotes the proliferation of myeloid cell lines and enhances erythroid burst formation by normal murine bone marrow cells in vitro

Blood ◽  
1990 ◽  
Vol 76 (5) ◽  
pp. 906-911 ◽  
Author(s):  
DE Williams ◽  
PJ Morrissey ◽  
DY Mochizuki ◽  
P de Vries ◽  
D Anderson ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
Cell Lines ◽  
Bone Marrow Cells ◽  
Myeloid Cell ◽  
Murine Bone Marrow ◽  
T Cell Growth Factor ◽  
Marrow Cells

T-cell growth factor P40 was examined for possible effects on murine interleukin-3 (IL-3)-dependent myeloid cell lines and freshly isolated murine bone marrow cells. The results showed that P40 stimulated the proliferation of some IL-3-dependent myeloid cell lines of both early myeloid and mast cell phenotype and synergized with IL-3. P40 did not promote proliferation of fresh bone marrow cells, bone marrow enriched for early myeloid cells by 5-fluorouracil treatment, or bone marrow derived mast cells as assessed in 3H-TdR incorporation assays. P40 did not influence the growth of murine colony-forming unit granulocyte- macrophage in agar cultures, either alone or in the presence of optimal or sub-optimal concentrations of CSF-1, GM-colony-stimulating factor, or IL-3. P40 did potentiate burst-forming unit-erythroid (BFU-E) formation in the presence of erythropoietin; however, this was dependent on the cell plating density, suggesting an indirect stimulation of BFU-E by P40. The indirect nature of P40 action on BFU-E was further demonstrated in cell separation experiments and indicated that the effect was mediated by T cells. These data expand the repertoire of cells that P40 influences.

scholarly journals A bone marrow stromal cell line is a source and target for platelet- derived growth factor

Blood ◽  
1993 ◽  
Vol 81 (10) ◽  
pp. 2547-2553 ◽  
Author(s):  
SL Abboud
Keyword(s):  
Bone Marrow ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Stromal Cell ◽  
Transforming Growth Factor ◽  
Platelet Derived Growth Factor ◽  
Northern Analysis ◽  
Tgf Beta ◽  
Binding Studies ◽  
A Chain

Abstract Platelet-derived growth factor (PDGF) stimulates multipotent and erythroid progenitors as well as stromal fibroblasts. Any of the three dimeric forms of PDGF (AA, AB, or BB) could potentially interact with these cells; however, the precise cellular origin of PDGF production in the bone marrow microenvironment is not known. In the present study, we found that medium conditioned by MBA-2, murine bone marrow-derived endothelial cells, contains PDGF activity that competes for [125I]PDGF binding to human foreskin fibroblasts and is mitogenic for these fibroblasts. Northern analysis of poly(A)+ RNA from MBA-2 shows the expression of both PDGF A-chain and B-chain mRNAs. Because cytokines such as transforming growth factor-beta (TGF-beta) regulate hematopoiesis and stimulate PDGF in certain mesenchymal cells, we determined whether TGF-beta influences PDGF secretion and gene expression in MBA-2. TGF-beta induced PDGF A-chain and B-chain mRNAs and the release of PDGF activity. Each of the three PDGF isoforms also stimulated DNA synthesis in MBA-2, but with different potency (BB = AB = AA). Ligand binding studies showed specific binding of labeled PDGF BB and, to a lesser extent, PDGF AA isoform, consistent with predominant expression of the PDGF-beta receptor in MBA-2. These data show that murine endothelial stromal cells release PDGF activity and respond to PDGF. Local production of PDGF in the marrow microenvironment may play an important role in regulating hematopoietic and stromal cell proliferation.

scholarly journals Insulin-like growth factor-I regulates pro-B cell differentiation

Blood ◽  
1992 ◽  
Vol 80 (5) ◽  
pp. 1207-1212 ◽  
Author(s):  
KS Landreth ◽  
R Narayanan ◽  
K Dorshkind
Keyword(s):  
Bone Marrow ◽  
Biological Activity ◽  
Cell Differentiation ◽  
B Cells ◽  
Growth Factor ◽  
Heavy Chain ◽  
Stromal Cell ◽  
B Cell Differentiation ◽  
Factor I ◽  
Igf I

Abstract Progression of B-lymphocyte development in the bone marrow of postnatal mammals is marked by progressive rearrangement and expression of immunoglobulin (Ig) heavy- and light-chain genes. Following productive VHDJH gene rearrangement in the Ig heavy-chain gene complex, mu-heavy chain is the first Ig gene product expressed in cells committed to the B-lymphoid differentiation pathway. Interleukin (IL)-7 has been shown to stimulate proliferation of pre-B cells following c mu expression and this proliferative stimulus is potentiated by kit ligand (KL). However, it appears that neither of these cytokines contributes to differentiation of pro-B cells or initiation of expression of Ig gene products. We previously demonstrated that differentiation of pro-B cells and expression of mu-heavy chain is stimulated by either bone marrow stromal cell line S17 or cell-free supernatants from that line. This biological activity was attributed to molecules with an apparent M(r) of less than 10 Kd and approximately 40 to 60 Kd. We now report that this biological activity resides with stromal cell-derived insulin- like growth factor-I (IGF-I). Recombinant IGF-I stimulated the expression of cytoplasmic mu-heavy chain in short-term bone marrow cultures and this stimulus was abrogated in the presence of anti-IGF-I antibody. We also demonstrate that either anti-IGF-I antibody or pretreatment of S17 cells with antisense oligonucleotide for IGF-I abrogated the pro-B cell differentiation activity of S17 stromal cell supernatants. Although IGF-I did not directly stimulate proliferation of B-lineage cells, like KL, it potentiated the proliferative stimulus provided by IL-7. Taken together, these data strongly suggest that IGF- I produced by bone marrow stromal cells in the hematopoietic microenvironment plays a key role in regulating primary B lymphopoiesis.

scholarly journals Stem cell factor and basic fibroblast growth factor are synergistic in augmenting committed myeloid progenitor cell growth

Blood ◽  
1994 ◽  
Vol 83 (4) ◽  
pp. 907-910 ◽  
Author(s):  
JL Gabrilove ◽  
K White ◽  
Z Rahman ◽  
EL Wilson
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
Fibroblast Growth Factor ◽  
Stromal Cells ◽  
Stem Cell Factor ◽  
Progenitor Cell ◽  
Fibroblast Growth ◽  
Gm Csf

Abstract Stem cell factor (SCF) and basic fibroblast growth factor (bFGF) are hematopoietic cytokines produced by bone marrow stromal cells. It is known that, although SCF and bFGF have limited clonogenic activity on their own, they can augment colony-stimulating factor (CSF)-mediated progenitor cell growth. Because these factors are both sequestered by stromal cells, we examined their interaction on progenitor cell growth in conjunction with granulocyte-macrophage-CSF (GM-CSF). In this study, we show that clonogenic growth derived from low-density bone marrow cells stimulated by GM-CSF is significantly augmented (P < .001) in the presence of maximal (100 ng/mL) concentrations of SCF in combination with 100 ng/mL of bFGF. When CD34+ cells are used, the synergistic effect of bFGF and SCF for GM-CSF-mediated progenitor cell growth is further increased, resulting in as much as a sevenfold increase in detectable colony-forming units granulocyte-macrophage (P < .001). These data suggest that the synergistic activity of bFGF and SCF is mediated directly on hematopoietic precursors. These observations suggest that bFGF and SCF, concentrated locally on stromal cell surfaces, might interact in concert with other hematopoietic cytokines to regulate stem cell proliferation and differentiation in hematopoietic niches in the bone marrow.

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