The fractionation, characterization, and subcellular localization of colony-stimulating activities released by the human monocyte-like cell line, GCT

DiPersio, JF; Brennan, James K.; Ma, Lichtman; Abboud, CN; Kirkpatrick, Francis H.

doi:10.1182/blood.v56.4.717.bloodjournal564717

Cited by 8 publications

(9 citation statements)

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“…Thereafter, 1 x lo5 normal nonadherent marrow cells in agar medium were overlayered, the plates incubated under standard conditions Abboud et al, 19801, and colonies counted on days 7 and 14. In other studies, supernates from HL-60 cells cultured in the presence of 0-1.5% DMSO were studied for GM-CSF by incorporation into single-layer, methylcellulose cultures of normal, nonadherent marrow cells (Collins et al, 1978;DiPersio et al, 1980) and also for the ability to stimulate 3HTdr incorporation into HL-60 microcultures containing 0-1.5% DMSO as described above.…”

Section: Hl-60 Cell Maturationmentioning

confidence: 99%

Interactions of dimethyl sulfoxide and granulocyte‐macrophage colony‐stimulating factors on the growth and maturation of HL‐60 cells

Brennan

Lee

Abboud

et al. 1987

Journal Cellular Physiology

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We have studied the interactions of dimethyl sulfoxide (DMSO), Giant Cell Tumor (GCT) cell-conditioned medium (GCT CM), and highly purified granulocyte-macrophage colony-stimulating factors (GM-CSF) on the growth and maturation of a highly passaged population of HL-60 cells. DMSO produced dose-dependent inhibition of HL-60 growth in liquid and semisolid media. Growth was partially to completely restored by the addition of GCT CM to cultures. Experiments in which cell volume, cell cycle kinetics, tritiated thymidine (3HTdr) incorporation, cell number, and nitroblue tetrazolium (NBT) reduction were compared during culture indicated that DMSO inhibited the spontaneous increase in cell volume and flow of cells through the cell cycle which occurred in the first day of culture, the increase in 3HTdr incorporation which was detectable by day 2; and the increment in cell counts which occurred by day 3. These effects were opposed by GCT CM. In contrast, the DMSO-induced increase in NBT reduction which occurred by day 6 was not influenced by GCT CM. The major principle opposing DMSO was GM-CSF, since (1) highly purified GM-CSF from GCT cells and recombinant GM-CSF from COS cells transfected with the Mo cell GM-CSF gene overcame greater than 50% of DMSO inhibition; and (2) conditioned media from cells not producing CSF, G-CSF from GCT cells, and recombinant G-CSF from Escherichia coli transfected with the G-CSF gene from 5,637 cells were inactive. DMSO had little or no effect on the elaboration of autostimulatory activity by HL-60 cells. DMSO is a useful agent for inhibiting the spontaneous growth of HL-60 cells and restoring their dependence on GM-CSF, a property which may be mediated through the effects of DMSO on cell cycle kinetics and/or maturation.

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Section: Hl-60 Cell Maturationmentioning

confidence: 99%

Interactions of dimethyl sulfoxide and granulocyte‐macrophage colony‐stimulating factors on the growth and maturation of HL‐60 cells

Brennan

Lee

Abboud

et al. 1987

Journal Cellular Physiology

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“…Mononucleated cells from bone marrow or peripheral blood were separated by density-gradient centrifugation (30 min at 400g) using Ficoll-Hypaque (1.077 g/ml). Two X lo5 cells were incubated in semisolid culture medium containing 20% fetal calf serum (FCS), 10% giant cell tumor-conditioned medium (GCT-CM, GIBCO) as colony-stimulating factor, and 0.3% agar in alphamedium (a-MEM), and were then cultured for 14 days at 37°C in 5% CO, in air for CFU-GM [9]. Colonies with more than 50 cells were counted as CFU-GM.…”

Section: Assay For Hemopoietic Progenitor Cellsmentioning

confidence: 99%

Detecting of the minimal residual disease contaminated in peripheral blood stem cell transplantation in the B‐Cell malignant lymphoma patients

et al. 1992

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For sufficient collection of hemopoietic stem cells from peripheral blood for autologous peripheral blood stem cell transplantation (PBSCT), four patients with B-cell-type non-Hodgkin lymphoma (B-NHL) were examined for the appearance of circulating hemopoietic progenitors in blood (PSC) during the hemopoietic recovery phase following marrow ablative therapy in combination with or without administration of recombinant human granulocyte colony-stimulating factor (rhG-CSF). Each patient received only chemotherapy in the first course, and rhG-CSF (1 microgram/kg/day) was administered for 14 consecutive days from the last day of the second chemotherapy. In the second chemotherapy course with rhG-CSF administration, white blood cell (WBC) counts demonstrated two peaks, and the appearance of granulocyte-macrophage precursor cells (CFU-GM) in blood at the maximum level was coincident with the second peak of WBC elevation. Erythroid precursor cells (BFU-E) were also detectable in blood after chemotherapy but the peak level was not enhanced by the use of rhG-CSF. To determine whether the minimal residual disease (MRD) cells were contaminated in PSC corrected from blood, kappa-lambda imaging (KLI) analysis was performed to detect the malignant B-cell population (mBp) before and after chemotherapy. No mBp was found in two of four patients in blood, although three of them were involved with mBp in bone marrow. The presence of mBp was detected in two patients both before and after chemotherapy, even though these cells were hardly detected morphologically, suggesting the necessity of judging for the incidence of contamination of MRD cells when collecting PSCs.

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“…Mononuclear human blood cells (5 x 10S/ml) or bone marrow cells (105/ml) were cultured for 14 d in 0.3% agar (Bacto-Agar, Difco), in McCoy's 5A or CMRL 1066 medium, with 18% FCS. BMC cultures were stimulated with 0.1 ml of GCT (Gibco) which contains a CSF produced by an established human monocyte-like cell line (13). Blood cell cultures were run with or without GCT, which made no difference.…”

Section: Gy-cfc Assaymentioning

confidence: 99%

Thymidine‐dependent effect of granulocyte‐derived inhibitor on granulocyte‐macrophage progenitor cells (GM‐CFC)

Bøyum

Helgestad

Løvhaug

1988

European J of Haematology

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We have compared the effect of granulocyte extract (GRE) on proliferation of hemopoietic cells from various sources, using two different cultures media, CMRL 1066 and McCoy 5A. GRE caused a strong (80-90%) inhibition of granulocytemacrophage colony forming cells (GM-CFC) in cultures with medium CMRL 1066. GM-CFC in human blood and human and mouse bone marrow were equally sensitive to the inhibitor. The inhibitor had a maximal effect in the concentration range corresponding to GRE from 2 x lo-' to 2 x 106 cells per 1 ml culture dish. At higher GRE concentration the inhibition was reduced. GM-CFC from human blood and mouse marrow were suppressed in cultures with McCoy's medium as well, but to a lesser extent than in CMRL 1066 cultures. On the other hand, in cultures with human bone marrow cells (BMC) and McCoy's medium, GRE had no inhibitory effect. CMRL 1066 medium contains a number of components not present in McCoy's medium. In a systematic study where these substances were added one by one toMcCoy's medium we found that inhibition by GRE depended upon the presence of thymidine. At a thymidine concentration of 3 x molA GRE strongly suppressed GM-CFC in human blood and bone marrow. This thymidine concentration itself had no effect. Other nucleosides or components of the CMRL 1066 did not potentiate the suppressive effect of GRE.

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The fractionation, characterization, and subcellular localization of colony-stimulating activities released by the human monocyte-like cell line, GCT

Cited by 8 publications

References 0 publications

Interactions of dimethyl sulfoxide and granulocyte‐macrophage colony‐stimulating factors on the growth and maturation of HL‐60 cells

Interactions of dimethyl sulfoxide and granulocyte‐macrophage colony‐stimulating factors on the growth and maturation of HL‐60 cells

Detecting of the minimal residual disease contaminated in peripheral blood stem cell transplantation in the B‐Cell malignant lymphoma patients

Thymidine‐dependent effect of granulocyte‐derived inhibitor on granulocyte‐macrophage progenitor cells (GM‐CFC)

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