Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:BIOD00035 (CSF)
 30,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Granulocyte-macrophage colony stimulating factor (GM-CSF) from mouse lung conditioned medium has recently been purified. This GM-CSF was radioiodinated using the chloramine T method, but dimethylsulfoxide was needed to prevent the loss of biological activity during the iodination. 125I-labeled GM-CSF was isolated from the reaction mixture by gel filtration and affinity chromatography with concanavalin A-Sepharose. One hour after intravenous injection of 125I-labeled GM-CSF almost 80% of the radioactivity was still localized in the serum. 125I-labeled GM-CSF was cleared from the blood of C57BL mice with a serum half-life of 7.3 +/- 1.3 hours. Six hours after intravenous injection 125I-GM-CSF appeared to be distributed throughout most of the tissues of C57BL mice. There was no selective concentration of 125I-labeled GM-CSF in the bone marrow, but levels in the kidney were three times higher than expected from the distribution of 125I-labeled mouse serum albumin. 125I detected in the blood 6 hours after injection of 125I-labeled GM-CSF was precipitable with trichloroacetic acid and bound to concanavalin A-Sepharose. 125I detected in the urine was not macromolecular and appeared to result from the degradation of 125I-labeled GM-CSF.
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PMID:Serum half-life and organ distribution of radiolabeled colony stimulating factor in mice. 30 12

A colony-stimulating factor (M-CSF) has been partially purified and concentrated from mouse yolk sac-conditioned medium (YSCM). M-CSF appeared to preferentially stimulate CBA bone marrow granulocyte-macrophage progenitor cells (GM-CFC) to differentiate to form macrophage colonies in semisolid agar cultures. By comparison, colony-stimulating factor (GM-CSF) from mouse lung-conditioned medium (MLCM) stimulated the formation of granulocytic, mixed granulocytic-macrophage, and pure macrophage colonies. Mixing experiments indicated that both M-CSF and GM-CSF stimulated all of the GM-CFC but that the smaller CFC were more sensitive to GM-CSF and that the larger CFC were more sensitive to M-CSF. Almost all developing "clones" stimulated initially with M-CSF continued to develop when transferred to cultures containing GM-CSF. In the converse situation, only 50% of GM-CSF prestimulated "clones" survived when transferred to cultures containing M-CSF. All clones initially stimulated by M-CSF or transferred to cultures stimulated by M-CSF contained macrophages after 7 days of culture. These results suggest that there is a population of cells (GM-CFC) that are capable of differentiating to form both granulocytes and macrophages, but, once these cells are activated by a specific CSF (e.g. M-CSF), they are committed to a particular differentiation pathway. The pattern of CFC differentiation was not directly related to the rate of proliferation: cultures maximally stimulated by M-CSF produced mostly macrophage colonies, but the presence of small amounts of GM-CSF produced granulocytic cells in 30% of the colonies. Gel filtration, polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate, and affinity chromatography with concanavalin A-Sepharose indicated that M-CSF from yolk sacs was a glycoprotein with an apparent molecular weight of 60,000. There was some heterogeneity of the carbohydrate portion of the molecule as evidenced by chromatography on concanavalin A-Sepharose.
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PMID:Molecular and biological properties of a macrophage colony-stimulating factor from mouse yolk sacs. 30 1

We previously reported a dramatically increased number of macrophages in tumor-bearing mice. In this study, we investigated the involvement of CSF in that phenomenon. CSF-1 responding cells as macrophages precursors increased significantly in number in the spleens of tumor-bearing mice as compared with those in normal mice. Splenic cells and sera from the tumor-bearing mice respectively expressed CSF-1 in mRNA and serum protein levels, but failed to express the other CSF (granulocyte-macrophage-CSF or IL-3). Nonadherent splenic mononuclear cells (< 0.5% macrophages) from normal mice proliferated and differentiated into mature macrophages in culture within 7 days with recombinant mouse CSF-1 (rCSF-1). Both macrophages harvested from tumor-bearing mice and those activated in vitro with rCSF-1 expressed mostly Mac-1, -2 (and -3) Ag, showed yeast phagocytosis, produced IL-1 but not IL-2 or IL-3, and displayed potent cytotoxicity against NK cell resistant Meth-A tumor cells. These macrophages also expressed lipocortin I mRNA and secreted lipocortin I protein, and suppressed mitogenic responses of splenic lymphocytes. rCSF-1-activated macrophages derived from nonadherent splenic cells expressed both CSF-1 and CSF-1 receptor (c-fms) mRNA. Administration of rCSF-1 into normal mice induced hemopoietic and immunologic alternations similar to those observed in tumor-bearing mice. These results suggest that CSF-1 is involved in the dramatic increase of macrophages in tumor-bearing mice, possibly through an autocrine or paracrine loop.
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PMID:Role of colony-stimulating factor-1 in macrophage activation in tumor-bearing mice. 128 Nov 98

The kinetics of GM-CSF and G-CSF secretion by purified adherent human monocytes were studied by quantitative immunoassays. Interleukin-1 (IL-1); 4-40 ng/ml and E. coli lipopolysaccharide (LPS); 0.1-1.00 ng/ml, were the most effective stimuli and induced dose-dependent secretion of both GM-CSF and G-CSF. Secretion of newly synthesized CSF was detectable 3-6 hours after stimulation and continued for approximately 24 h. Twenty minutes pulse exposure to LPS was sufficient to induce half maximum secretion of GM-CSF, and after 24-36 h the adherent monocytes could not be restimulated. Neither GM-CSF nor TNF could down-regulate the secretion of GM-CSF. IL-3 induced a minor secretion of GM-CSF whereas TNF, G-CSF, M-CSF and IFN-gamma were unable to induce GM-CSF secretion. In addition to LPS and IL-1, GM-CSF and to a minor degree TNF induced G-CSF secretion. Enriched T lymphocytes secreted GM-CSF, but not G-CSF, after stimulation with PHA or staphylococcal enterotoxin A (SEA), whereas LPS and IL-1 were without stimulatory effects. We also noted that enriched T lymphocytes added to LPS-stimulated adherent monocytes at ratios of 1:10 or more inhibited, in a dose-dependent fashion, GM-CSF secretion by 13-55%. These findings add new quantitative data on CSF secretion by human monocytes.
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PMID:Granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) secretion by adherent monocytes measured by quantitative immunoassays. 128 54

The ability of murine Steel factor to promote the in vitro production of granulocyte-macrophage progenitor cells (CFU-GM) was examined in short-term liquid cultures. Bone marrow from C57BL/6J or Sl/Sld mice was placed in culture for seven days with either Steel factor alone or in the presence of IL-3. CFU-GM responsive to GM-CSF, IL-3, and CSF-1 were measured in the input population and again after 3 or 7 days in culture. Steel factor alone increased the number of all CFU-GM types as early as 3 days after culture initiation, with further increases at day 7. This effect was potentiated by the addition of IL-3. Production of CFU-GM by C57BL/6J or Sl/Sld marrow was comparable except for enhanced production of CSF-1 responsive progenitors by Sl/Sld marrow. A recombinant Sld protein was also shown to be equivalent to the wild-type protein in its capacity to promote CFU-GM production from normal bone marrow.
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PMID:Recombinant murine steel factor stimulates in vitro production of granulocyte-macrophage progenitor cells. 128 17

We have established cell lines from a large cell carcinoma of the lung accompanied by marked granulocytosis and thrombocytosis, and have analyzed the factors with colony stimulating factor (CSF) activity produced by them. Analysis of the CSF activity present in the culture medium of the established cell lines demonstrated growth-stimulating activity on CMK cells, a human megakaryoblastic cell line and mouse bone marrow cells. A neutralization test with antibodies against G-, M- and GM-CSF indicated the stimulation for the proliferation of CMK and mouse bone marrow cells to be mediated partially by the CSFs. Furthermore, the measurement of GM-CSF and interleukin(IL)6 by enzyme-linked immunosorbent assay (ELISA) and northern blotting analysis indicated productions of G-, GM- and M-CSF and of IL6 from the cell lines but failed to exhibit IL3 gene expression. It is suggested that the cell lines could be of use in the study of CSFs and, also, that lymphokines act on leukocyte and platelet progenitor cells.
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PMID:Establishment of large cell lung cancer cell lines secreting hematopoietic factors inducing leukocytosis and thrombocytosis. 128 95

The pattern of changes in neutrophil myeloperoxidase (MPO) before, during and after bacteraemia was studied in 34 patients recovering from autologous bone marrow transplantation for relapsed Hodgkin's disease and non Hodgkin's lymphomas. Thirteen patients received haemopoietic growth factors (7 received M-CSF, 3 received G-CSF and 3 GM-CSF). The mean peroxidase index (MPXI) produced as part of a routine FBC performed by a flow cytochemistry blood autoanalyser (Technicon H*1) was used as a parameter to assess the MPO and subsequently the azurophil degranulation. The manufacturer's normal values for MPXI range from -10 to +10. Median MPXI on the day of documented bacteraemia was just below normal in the control and M-CSF groups (-10.8 and -8.9 respectively), but it was much below normal in the G-CSF (-16.5, P < 0.05) and even lower in the GM-CSF group (-39.6, P < 0.02); this correlated well with the decreased bacteraemia incidence in the last two groups. Although contact of neutrophils with bacterial chemoattractants resulted in primary degranulation in all groups, the pattern of changes in MPO content was different, suggesting that neutrophils primed in vivo with various haemopoietins respond to the challenge of microbial agents via different pathways.
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PMID:Patterns of primary degranulation as indicated by the mean myeloperoxidase index (MPXI) during bacteraemia in lymphoma transplants treated with growth factors. 128 46

We studied the biological characteristics of CD7+ acute myelogenous leukaemia (AML). We diagnosed nine out of 88 consecutive AML cases as CD7+ AML based on myeloperoxidase positivity and surface antigen expression. In eight of these nine cases more than 20% of leukaemic blasts were found to coexpress both CD7 and a myeloid-associated antigen, CD33, by a two-colour flow-cytometric assay, while in the remaining case more than 90% of blasts were positive for CD7 and myeloperoxidase. CD7+ AML was most frequently observed in M1 among AML subtypes according to the FAB classification. An early stage-specific antigen, CD34 was also expressed on leukaemic blasts from eight of these nine cases. Neither the T-cell receptor (TcR)-beta nor the TcR-gamma gene was clonally rearranged in any of the cases. We then studied the proliferative responses to stimulation by various growth factors. Among interleukin-3 (IL-3), granulocyte/macrophage colony-stimulating factor (GM-CSF), and granulocyte-CSF (G-CSF), IL-3 showed the strongest stimulatory effect on DNA synthesis and leukaemic blast colony formation in 8/9 and 6/8 CD7+ AML cases examined, respectively. On the other hand, the strongest stimulatory effect exerted by IL-3 on blast colony formation was observed in only six out of the 33 CD7- AML cases examined. Furthermore, CD7+ AML blasts could proliferate in response to stem cell factor (SCF); SCF alone showed stimulatory effects on blast colony formation (7/8 cases), and in 5/7 SCF-responding cases, stimulatory effects of SCF were more potent than those of IL-3. In addition, SCF enhanced blast colony formation synergistically with IL-3 in four of these seven cases. These data suggest that progenitor cells of CD7+ AML may possess the biological properties characteristic of immature haematopoietic stem cells.
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PMID:Biological characteristics of CD7 positive acute myelogenous leukaemia. 128 77

Retrovirally expressed human CSF-1 receptor can induce CSF-1-dependent growth of IL-3-dependent hemopoietic cells FDC-P1. Here we show that expression of the human CSF-1 receptor also allowed FDC-P1 cells to grow in response to Insulin-like Growth Factor-1 (IGF-I). The authentic receptor for IGF-I was identified by affinity cross-linking and binding analysis on both control (infected with a neo vector) and CSF-1 receptor expressing FDC-P1 cells. DNA and RNA analysis of these cells and of five clones of IGF-I responsive cells demonstrated that the IGF-I receptor gene was not rearranged nor was it abnormally expressed in IGF-I responsive cells. These results suggest that myeloid cells over-expressing CSF-1R (c-fms protooncogene product) might have a proliferative advantage over normal myeloid cells in a physiological situation, independently of the presence of CSF-1 or the capacity of the cells to respond to CSF-1. This would indicate a possible role for c-fms in human neoplasia.
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PMID:Insulin-like growth factor-1 stimulates proliferation of myeloid FDC-P1 cells overexpressing the human colony-stimulating factor-1 receptor. 128 71

In vitro proliferative response of the blast cells from 21 AML patients to hematopoietic growth factors (IL-3, GM-CSF, G-CSF and MCSF) was investigated. Proliferation of AML cells in the majority of cases was induced or promoted by one or more CSFs, among which the stimulation of IL-3 was the most effective. Spontaneous proliferation of the blast cells was also observed in half of the cases and could be inhibited as well as promoted by some CSFs. It is suggested that in vitro proliferation of AML cells varies from patient to patient and that CSF plays important roles in leukemogenesis.
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PMID:[Effects of various recombinant human hematopoietic growth factors on proliferation of blast cells in acute myeloid leukemia in vitro]. 128 86


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