scholarly journals Effects of 12-0-tetradecanoylphorbol-13-acetate (TPA) on the proliferation of granulocyte-macrophage colony-forming cells

Blood ◽  
1983 ◽  
Vol 61 (3) ◽  
pp. 575-579 ◽  
Author(s):  
AW Burgess ◽  
NA Nicola
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Fetal Liver ◽  
Mouse Bone Marrow ◽  
Gm Csf ◽  
Accessory Cells ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Csf Production ◽  
Number Of Cells

Abstract It has been suggested that 12–0-tetradecanoylphorbol-13-acetate (TPA) may stimulate the proliferation of granulocyte-macrophage (GM) colony- forming cells (CFC) via the GM colony-stimulating factor (CSF) receptor. GM-CFC in unfractionated mouse bone marrow and light density fetal liver (LDFL) cells were induced by TPA to form colonies in the absence of exogenously added GM-CSF. The colonies induced by TPA (10(- 8)M) were smaller than normally seen with maximal concentrations of GM- CSF, and less than 30% of the GM-CFC formed colonies in the presence of TPA. The number of colonies stimulated by TPA in the absence of GM-CSF was dependent on the number of cells plated. When fewer than 10,000 bone marrow cells or 3000 LDFL cells were plated in the 1-ml semisolid agar cultures, no colonies were stimulated by the TPA. Similarly, GM- CFC purified from the LDFL cells stimulated with TPA did not form colonies. However, when the fetal liver accessory cells (macrophages) were recombined with cell-sorter-purified GM-CFC, colony formation was again observed in the presence of TPA (10(-7)-10(-8) M). The number of colonies formed from the CFC was dependent on the number of accessory cells present, suggesting that the macrophages were induced by TPA to produce CSF. Although the purified GM-CFC required CSF for proliferation, TPA (10(-8) M) increased (5–10-fold) the sensitivity of the GM-CFC to GM-CSF. These observations indicate that TPA does not stimulate GM-CFC proliferation directly, but rather by inducing GM-CSF production by accessory cells and by increasing the responsiveness of GM-CFC to GM-CSF.

scholarly journals Effects of 12-0-tetradecanoylphorbol-13-acetate (TPA) on the proliferation of granulocyte-macrophage colony-forming cells

Blood ◽  
1983 ◽  
Vol 61 (3) ◽  
pp. 575-579
Author(s):  
AW Burgess ◽  
NA Nicola
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Fetal Liver ◽  
Mouse Bone Marrow ◽  
Gm Csf ◽  
Accessory Cells ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Csf Production ◽  
Number Of Cells

It has been suggested that 12–0-tetradecanoylphorbol-13-acetate (TPA) may stimulate the proliferation of granulocyte-macrophage (GM) colony- forming cells (CFC) via the GM colony-stimulating factor (CSF) receptor. GM-CFC in unfractionated mouse bone marrow and light density fetal liver (LDFL) cells were induced by TPA to form colonies in the absence of exogenously added GM-CSF. The colonies induced by TPA (10(- 8)M) were smaller than normally seen with maximal concentrations of GM- CSF, and less than 30% of the GM-CFC formed colonies in the presence of TPA. The number of colonies stimulated by TPA in the absence of GM-CSF was dependent on the number of cells plated. When fewer than 10,000 bone marrow cells or 3000 LDFL cells were plated in the 1-ml semisolid agar cultures, no colonies were stimulated by the TPA. Similarly, GM- CFC purified from the LDFL cells stimulated with TPA did not form colonies. However, when the fetal liver accessory cells (macrophages) were recombined with cell-sorter-purified GM-CFC, colony formation was again observed in the presence of TPA (10(-7)-10(-8) M). The number of colonies formed from the CFC was dependent on the number of accessory cells present, suggesting that the macrophages were induced by TPA to produce CSF. Although the purified GM-CFC required CSF for proliferation, TPA (10(-8) M) increased (5–10-fold) the sensitivity of the GM-CFC to GM-CSF. These observations indicate that TPA does not stimulate GM-CFC proliferation directly, but rather by inducing GM-CSF production by accessory cells and by increasing the responsiveness of GM-CFC to GM-CSF.

scholarly journals Effect of mouse interferon on growth and differentiation of mouse bone marrow cells stimulated by two different types of colony-stimulating factor

Blood ◽  
1983 ◽  
Vol 62 (3) ◽  
pp. 597-601 ◽  
Author(s):  
Y Yamamoto-Yamaguchi ◽  
M Tomida ◽  
M Hozumi
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Mouse Bone Marrow ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Mouse Bone Marrow Cells ◽  
Marrow Cells

Abstract The effects of mouse L-cell interferon (IFN) on growth of mouse bone marrow cells and their differentiation into macrophages and granulocytes were investigated in a liquid suspension culture system with two different types of colony-stimulating factor (CSF). Within 7 days, most bone marrow cells differentiated into macrophages in the presence of macrophage colony-stimulating factor (M-CSF) derived from mouse fibroblast L929 cells, but into both granulocytes (40%) and macrophages (23%) in the presence of a granulocyte-macrophage colony- stimulating factor (GM-CSF) from mouse lung tissue. IFN inhibited growth of bone marrow cells with both M-CSF and GM-CSF, but had 20 times more effect on bone marrow cells stimulated with M-CSF than on those stimulated with GM-CSF. A low concentration of IFN (50 IU/ml) stimulated production of macrophages by GM-CSF in liquid culture medium, whereas it selectively inhibited colony formation of macrophages in semisolid agar culture. IFN caused no detectable block of late stages of differentiation; mature macrophages and granulocytes were produced even when cell proliferation was inhibited by IFN. These results indicate that IFN preferentially affects growth and differentiation of the cell lineage of macrophages among mouse bone marrow cells.

scholarly journals Effect of mouse interferon on growth and differentiation of mouse bone marrow cells stimulated by two different types of colony-stimulating factor

Blood ◽  
1983 ◽  
Vol 62 (3) ◽  
pp. 597-601 ◽  
Author(s):  
Y Yamamoto-Yamaguchi ◽  
M Tomida ◽  
M Hozumi
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Mouse Bone Marrow ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Mouse Bone Marrow Cells ◽  
Marrow Cells

The effects of mouse L-cell interferon (IFN) on growth of mouse bone marrow cells and their differentiation into macrophages and granulocytes were investigated in a liquid suspension culture system with two different types of colony-stimulating factor (CSF). Within 7 days, most bone marrow cells differentiated into macrophages in the presence of macrophage colony-stimulating factor (M-CSF) derived from mouse fibroblast L929 cells, but into both granulocytes (40%) and macrophages (23%) in the presence of a granulocyte-macrophage colony- stimulating factor (GM-CSF) from mouse lung tissue. IFN inhibited growth of bone marrow cells with both M-CSF and GM-CSF, but had 20 times more effect on bone marrow cells stimulated with M-CSF than on those stimulated with GM-CSF. A low concentration of IFN (50 IU/ml) stimulated production of macrophages by GM-CSF in liquid culture medium, whereas it selectively inhibited colony formation of macrophages in semisolid agar culture. IFN caused no detectable block of late stages of differentiation; mature macrophages and granulocytes were produced even when cell proliferation was inhibited by IFN. These results indicate that IFN preferentially affects growth and differentiation of the cell lineage of macrophages among mouse bone marrow cells.

scholarly journals Granulocyte/macrophage colony-stimulating factor and accessory cells modulate radioprotection by purified hematopoietic cells

2005 ◽  
Vol 201 (6) ◽  
pp. 853-858 ◽  
Author(s):  
Tamiko R. Katsumoto ◽  
Jennifer Duda ◽  
Andrew Kim ◽  
Zabihullah Wardak ◽  
Glenn Dranoff ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Fetal Liver ◽  
Hematopoietic Cells ◽  
Colony Stimulating Factor ◽  
Term Survival ◽  
Gm Csf ◽  
Accessory Cells ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Granulocyte/macrophage colony-stimulating factor (GM-CSF) promotes the survival, proliferation, and differentiation of myeloid lineage cells and regulates chemotaxis and adhesion. However, mice in which the genes encoding GM-CSF (Gmcsf) or the β common subunit of the GM-CSF receptor (βc) are inactivated display normal steady-state hematopoiesis. Here, we show that host GM-CSF signaling strongly modulates the ability of donor hematopoietic cells to radioprotect lethally irradiated mice. Although bone marrow mononuclear cells efficiently rescue Gmcsf mutant recipients, fetal liver cells and Sca1+ lin−/dim marrow cells are markedly impaired. This defect is partially attributable to accessory cells that are more prevalent in bone marrow. In contrast, Gmcsf-deficient hematopoietic stem cells demonstrate normal proliferative potentials. Short-term survival is also impaired in irradiated βc mutant recipients transplanted with fetal liver or bone marrow. These data demonstrate a nonredundant function of GM-CSF in radioprotection by donor hematopoietic cells that may prove relevant in clinical transplantation.

scholarly journals M-CSF and GM-CSF Regulation of STAT5 Activation and DNA Binding in Myeloid Cell Differentiation is Disrupted in Nonobese Diabetic Mice

2008 ◽  
Vol 2008 ◽  
pp. 1-8 ◽  
Author(s):  
B. Rumore-Maton ◽  
J. Elf ◽  
N. Belkin ◽  
B. Stutevoss ◽  
F. Seydel ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Differentiation ◽  
Myeloid Cell ◽  
Mouse Bone Marrow ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Nonobese Diabetic ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Defects in macrophage colony-stimulating factor (M-CSF) signaling disrupt myeloid cell differentiation in nonobese diabetic (NOD) mice, blocking myeloid maturation into tolerogenic antigen-presenting cells (APCs). In the absence of M-CSF signaling, NOD myeloid cells have abnormally high granulocyte macrophage colony-stimulating factor (GM-CSF) expression, and as a result, persistent activation of signal transducer/activator of transcription 5 (STAT5). Persistent STAT5 phosphorylation found in NOD macrophages is not affected by inhibiting GM-CSF. However, STAT5 phosphorylation in NOD bone marrow cells is diminished if GM-CSF signaling is blocked. Moreover, if M-CSF signaling is inhibited, GM-CSF stimulationin vitrocan promote STAT5 phosphorylation in nonautoimmune C57BL/6 mouse bone marrow cultures to levels seen in the NOD. These findings suggest that excessive GM-CSF production in the NOD bone marrow may interfere with the temporal sequence of GM-CSF and M-CSF signaling needed to mediate normal STAT5 function in myeloid cell differentiation gene regulation.

scholarly journals Interleukin-1 synergizes with granulocyte-macrophage colony-stimulating factor on granulocytic colony formation by intermediate production of granulocyte colony-stimulating factor

Blood ◽  
1989 ◽  
Vol 74 (7) ◽  
pp. 2398-2404 ◽  
Author(s):  
MR Schaafsma ◽  
JH Falkenburg ◽  
N Duinkerken ◽  
J Van Damme ◽  
BW Altrock ◽  
...  
Keyword(s):  
Bone Marrow Cells ◽  
Interleukin 1 ◽  
Colony Growth ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Accessory Cells ◽  
Granulocytic Colony ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Abstract Interleukin-1 (IL-1) was found to act synergistically with granulocyte- macrophage colony-stimulating factor (GM-CSF) on granulocytic colony growth of normal human bone marrow cells, depleted of mononuclear phagocytes and T lymphocytes. Using CD34/HLA-DR-enriched bone marrow cells we demonstrated that this activity of IL-1 was not a direct action on hematopoietic progenitor cells, but an effect of an intermediate factor produced by residual accessory cells in response to IL-1. Neutralization experiments using an anti-IL-6 antiserum showed that IL-1-induced IL-6 did not contribute to the observed synergy. Furthermore, IL-6 by itself had neither a direct stimulatory effect on CFU-GM colony growth, nor did it act synergistically with GM-CSF on granulocytic or monocytic colony formation. Neutralization experiments with an anti-G-CSF monoclonal antibody showed that IL-1-induced G-CSF production was responsible for the synergy with GM-CSF. Using combinations of G-CSF and GM-CSF this synergistic activity could be detected at concentrations of G-CSF as low as 0.1 ng/mL (10 U/mL). Our results indicate that IL-1, but not IL-6, stimulates the GM-CSF- dependent proliferation of relatively mature myeloid progenitor cells in the presence of small numbers of accessory cells.

scholarly journals Detection of a human CFC with a high proliferative potential

Blood ◽  
1989 ◽  
Vol 74 (2) ◽  
pp. 609-612 ◽  
Author(s):  
IK McNiece ◽  
FM Stewart ◽  
DM Deacon ◽  
DS Temeles ◽  
KM Zsebo ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Growth Period ◽  
Proliferative Potential ◽  
Cell Type ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Marrow Cells

Abstract Colony forming cells (CFC) with high proliferative potential have been detected in nutrient agar cultures of human bone marrow cells containing recombinant human interleukin-3 (IL-3) and granulocyte macrophage colony stimulating factor (GM-CSF). These CFC were detected by the formation of large colonies with diameters greater than 0.5 mm and containing approximately 50,000 cells after 28 days incubation. The incidence of these CFC was only two in 100,000 normal bone marrow cells; however, bone marrow from patients treated with 5-fluorouracil contained up to sevenfold higher numbers of these CFC. The characteristics of these CFC, multifactor-responsive progenitors with high proliferative potential, requiring a prolonged growth period in culture and showing a relative preservation in marrow from individuals pretreated with 5-fluorouracil, are consistent with a human cell type equivalent to the primitive murine progenitor termed HPP-CFC.

scholarly journals Detection of a human CFC with a high proliferative potential

Blood ◽  
1989 ◽  
Vol 74 (2) ◽  
pp. 609-612 ◽  
Author(s):  
IK McNiece ◽  
FM Stewart ◽  
DM Deacon ◽  
DS Temeles ◽  
KM Zsebo ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Growth Period ◽  
Proliferative Potential ◽  
Cell Type ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Marrow Cells

Colony forming cells (CFC) with high proliferative potential have been detected in nutrient agar cultures of human bone marrow cells containing recombinant human interleukin-3 (IL-3) and granulocyte macrophage colony stimulating factor (GM-CSF). These CFC were detected by the formation of large colonies with diameters greater than 0.5 mm and containing approximately 50,000 cells after 28 days incubation. The incidence of these CFC was only two in 100,000 normal bone marrow cells; however, bone marrow from patients treated with 5-fluorouracil contained up to sevenfold higher numbers of these CFC. The characteristics of these CFC, multifactor-responsive progenitors with high proliferative potential, requiring a prolonged growth period in culture and showing a relative preservation in marrow from individuals pretreated with 5-fluorouracil, are consistent with a human cell type equivalent to the primitive murine progenitor termed HPP-CFC.

scholarly journals Granulocyte-macrophage colony-stimulating factor requires interaction with accessory cells or granulocyte-colony stimulating factor for full stimulation of human myeloid progenitors

Blood ◽  
1989 ◽  
Vol 73 (2) ◽  
pp. 402-405
Author(s):  
D Ferrero ◽  
C Tarella ◽  
R Badoni ◽  
D Caracciolo ◽  
G Bellone ◽  
...  
Keyword(s):  
Bone Marrow Cells ◽  
Colony Growth ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Accessory Cells ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Reduced Activity ◽  
Stimulating Factor ◽  
Myeloid Progenitors

Human recombinant GM-CSF (rGM-CSF) was tested on highly purified and fractionated CFU-GM subsets. The fractionation was performed with the DS1–1 monoclonal antibody (MoAb), which distinguishes early and late CFU-GM. On whole bone marrow cells, rGM-CSF had a colony-stimulating activity comparable to that of known sources of CSFs, ie, the supernatant (SN) of TPA 30–1 or 5637 cell lines, used as control. A greatly reduced activity was observed when CFU-GM were depleted of phagocytizing and E rosetting cells (colony growth of 27% as compared with control). On fractionated CFU-GM, the rGM-CSF activity was even more reduced on both early and late progenitors (18% and 6% of colony growth, respectively). However, when rGM-CSF was used together with rG- CSF at suboptimal concentrations, the colony growth reached values analogous to that of control cultures. A synergistic interaction between rGM-CSF and rG-CSF in stimulating either early or late myeloid progenitors was observed. The results suggest that the activity of rGM- CSF on CFU-GM is mainly exerted through cooperation with accessory cells. r-G-CSF is one of the factors that can synergistically cooperate with r-GM-CSF in the myelopoietic stimulation.

scholarly journals Biosynthetic (recombinant) human granulocyte-macrophage colony- stimulating factor: effect on normal bone marrow and leukemia cell lines

Blood ◽  
1986 ◽  
Vol 67 (1) ◽  
pp. 31-36 ◽  
Author(s):  
M Tomonaga ◽  
DW Golde ◽  
JC Gasson
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Bone Marrow Cells ◽  
Leukemia Cell ◽  
Colony Stimulating Factor ◽  
Normal Peripheral Blood ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Abstract To examine the biologic properties of the molecule encoded by the human gene for granulocyte-macrophage colony-stimulating factor (GM-CSF), we expressed the cloned complementary DNA (cDNA) in transfected monkey COS cells and purified the resultant protein. Purified biosynthetic human GM-CSF was added to cultures of normal hematopoietic progenitor cells in semisolid media, and the resulting colonies were characterized cytochemically. Non-adherent light-density bone marrow cells from healthy adult volunteers were maximally stimulated with GM-CSF (approximately 250 pmol/L, and four types of colonies were consistently identified by aspirating the individual colonies and staining with a triple stain for specific and nonspecific esterases and eosinophilic granules. Pure neutrophilic granulocyte (G), mixed granulocyte- macrophage (GM), pure macrophage (M), and pure eosinophil (EO) colonies were observed, the mean incidences on day 8 being 70%, 20%, 5%, and 5%, and on day 14, 7.5%, 16.6%, 50.9%, and 25.0%, respectively. In all types of colonies, complete maturation to segmented forms or typical macrophages was detected. GM-CSF did not enhance the growth of BFU-E from normal peripheral blood buffy coat cells in the simultaneous presence of erythropoietin alone or erythropoietin with purified erythroid-potentiating activity. GM-CSF stimulated HL-60 and KG-1 colony formation twofold and fivefold, respectively; consistent differentiation induction towards monocytic and eosinophilic lineages was observed in HL-60 but not in KG-1. These in vitro findings indicate that GM-CSF is a multilineage stimulator for progenitor cells of G, GM, M, and EO colonies.

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