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CSF3  -  colony stimulating factor 3 (granulocyte)

Homo sapiens

Synonyms: C17orf33, CSF3OS, G-CSF, GCSF, Granulocyte colony-stimulating factor, ...
 
 
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Disease relevance of CSF3

 

Psychiatry related information on CSF3

 

High impact information on CSF3

  • In myeloid leukemia and myelodysplastic syndromes, CSF treatment, particularly G-CSF, has proved effective for certain patients in improving neutrophil, platelet, and occasionally red cell production while reducing blast cells [12].
  • BACKGROUND: In recipients of allogeneic hematopoietic-cell transplants, peripheral-blood cells mobilized with the use of filgrastim (recombinant granulocyte colony-stimulating factor) engraft more rapidly than bone marrow [13].
  • METHODS: We performed a randomized, double-blind, placebo-controlled trial of granulocyte colony-stimulating factor (G-CSF) in afebrile outpatients with severe chemotherapy-induced neutropenia [14].
  • The median time to an absolute neutrophil count of at least 500 per cubic millimeter was significantly shorter for patients who received G-CSF (two days, vs. four days for the patients given placebo) [14].
  • Among patients who did not have febrile neutropenia during the first week of G-CSF or placebo injections, higher systemic exposure to the growth factor on day 7 was significantly related to a lower probability of subsequent hospitalization (P=0.049) [15].
 

Chemical compound and disease context of CSF3

 

Biological context of CSF3

  • Granulocyte colony-stimulating factor (G-CSF) is a member of the CSF family of hormone-like glycoproteins that regulate haematopoietic cell proliferation and differentiation, and G-CSF almost exclusively stimulates the colony formation of granulocytes from committed precursor cells in semi-solid agar culture [20].
  • GM-CSF and G-CSF both induce a change from low to high-affinity neutrophil IgA Fc crystallizable fragment receptors within 30 min; a change which is associated with the development of IgA-mediated phagocytosis [21].
  • We have now determined the partial amino-acid sequence of the purified G-CSF protein, and by using oligonucleotides as probes, have isolated several clones containing G-CSF complementary DNA from the cDNA library prepared with messenger RNA from CHU-2 cells [20].
  • The complete nucleotide sequences of two of these cDNAs were determined and the expression of the cDNA in monkey COS cells gave rise to a protein showing authentic G-CSF activity [20].
  • Furthermore, Southern hybridization analysis of DNA from normal leukocytes and CHU-2 cells suggests that the human genome contains only one gene for G-CSF and that some rearrangement has occurred within one of the alleles of the G-CSF gene in CHU-2 cells [20].
 

Anatomical context of CSF3

  • The haematopoietic factors granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) prime neutrophils to be more responsive to a variety of stimuli [21].
  • We now report that treatment of endothelial cells (EC) with modified low-density lipoproteins obtained by mild iron oxidation or by prolonged storage, results in a rapid and large induction of the expression of granulocyte-macrophage colony-stimulating factor (GM-CSF), macrophage CSF (M-CSF) and granulocyte CSF (G-CSF) [22].
  • These growth factors affect the differentiation, survival, proliferation, migration and metabolism of macrophages/granulocytes, and G-CSF and GM-CSF also affect the migration and proliferation of EC [22].
  • Transcripts of the G-CSF, IL-1 alpha, and IL-1 beta genes were never detected in NK cells in these experiments [23].
  • Whereas a mixture of G-CSF, M-CSF, and IL 3 produced a mitogenic response in the prostatic carcinoma cells, these three factors were not present in our bone marrow samples in sufficient quantities to promote the observed proliferative response [24].
 

Associations of CSF3 with chemical compounds

  • The purified recombinant G-CSF runs as a single band with an apparent Mr of 19,000 on a polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate [25].
  • Exposure of normal mesothelial cells to epidermal growth factor (EGF), lipopolysaccharide (LPS), or tumor necrosis factor (TNF) induced expression of G-CSF mRNA [26].
  • Although the G-CSFR belongs to the cytokine receptor superfamily, which lacks an intracellular kinase domain, G-CSF-induced tyrosine phosphorylation of cellular proteins is critical for its biologic activities [27].
  • Granulocyte colony-stimulating factor (G-CSF) is a glycoprotein that stimulates proliferation and differentiation of progenitor cells of neutrophils by signaling through its receptor (G-CSFR) [27].
  • The combination of EGF and TNF induced threefold more G-CSF transcripts than did either factor alone [26].
  • We demonstrate that slanDCs (14.9 x 10(6)/L to 64.0 x 10(6)/L) are efficiently mobilized by G-CSF and retain their capacity to produce IL-12 and TNF-alpha at high levels [28].
 

Physical interactions of CSF3

  • Similarly, 125I-IL-8 ligand binding to PMN is increased by G-CSF and decreased by LPS treatment [29].
  • Analysis of the electrostatic potentials supports a recently proposed hetero-oligomeric model for a high-affinity IL-4 receptor and suggests a possible new receptor binding mode for G-CSF; it also provides valuable information for guiding structural and mutagenesis studies of signal-transducing proteins and their receptors [30].
  • A chimeric cytokine, myelopoietin-1, composed of daniplestim and a G-CSF receptor agonist binds both the IL-3 and G-CSF receptors [31].
  • The tax response of the G-CSF promoter requires not only the conserved CK-1 sequence but also an adjacent NF-IL6 binding site that may explain the cell restricted function of the G-CSF promoter [32].
  • Our cell-level model suggests that ligand depletion may be reduced in vitro by decreasing the endosomal affinity of endocytosed GCSF/GCSFR complexes, matching experimental findings [33].
 

Enzymatic interactions of CSF3

 

Regulatory relationships of CSF3

  • The proliferative effects of granulocyte colony-stimulating factor (G-CSF) and macrophage colony-stimulating factor (M-CSF) on human hematopoietic cells have been reported, but the intranuclear mechanism of early signal response to these mitogenic stimuli remains unknown [3].
  • Thus, these results indicate that one mechanism of the pathogenesis in SCN patients is reduced responsiveness of neutrophil progenitor cells to G-CSF and that SCF can enhance the responsiveness of these cells to G-CSF [37].
  • On the other hand, in six cases, G-CSF enhanced the IL-3- or GM-CSF-stimulated thymidine uptake [38].
  • Tumor necrosis factor alpha (TNF alpha) stimulates production of granulocyte colony-stimulating factor (G-CSF) protein and mRNA in fibroblast cells [39].
  • In other words, IL-4 may induce progenitor cells to become sensitive to G-CSF and thereby induce neutrophil differentiation [40].
 

Other interactions of CSF3

  • Together these data add to our understanding of the mechanisms of cytokine receptor signaling, emphasize the role of GCSFR mutations in the etiology of SCN, and implicate such mutations in G-CSF hyporesponsiveness [2].
  • G-CSF receptor numbers on purified blood granulocytes are also downmodulated by TNF [41].
  • In parallel with regrowth from the G0/G1 resting state by addition of recombinant human G-CSF or M-CSF after serum deprivation, NKM-1 cells showed the transient expression of the junB gene with a peak of ninefold above the basal level between 40 and 60 min [3].
  • However, pretreatment of patients with G-CSF with or without SCF did not enhance the retroviral infectability of growth factor-mobilized progenitor cells [42].
  • When 32D cells are switched to medium containing granulocyte colony-stimulating factor (G-CSF) instead of IL-3, D-type cyclins are degraded and, in the absence of their associated kinase activity, the cells arrest in the first gap phase (G1) of the cell cycle and differentiate to neutrophils [43].
 

Analytical, diagnostic and therapeutic context of CSF3

References

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  2. Novel point mutation in the extracellular domain of the granulocyte colony-stimulating factor (G-CSF) receptor in a case of severe congenital neutropenia hyporesponsive to G-CSF treatment. Ward, A.C., van Aesch, Y.M., Gits, J., Schelen, A.M., de Koning, J.P., van Leeuwen, D., Freedman, M.H., Touw, I.P. J. Exp. Med. (1999) [Pubmed]
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  18. The role of myelopoietic growth factors in managing cancer in the elderly. Balducci, L., Carreca, I. Drugs (2002) [Pubmed]
  19. Lenograstim. A review of its pharmacological properties and therapeutic efficacy in neutropenia and related clinical settings. Frampton, J.E., Yarker, Y.E., Goa, K.L. Drugs (1995) [Pubmed]
  20. Molecular cloning and expression of cDNA for human granulocyte colony-stimulating factor. Nagata, S., Tsuchiya, M., Asano, S., Kaziro, Y., Yamazaki, T., Yamamoto, O., Hirata, Y., Kubota, N., Oheda, M., Nomura, H. Nature (1986) [Pubmed]
  21. GM-CSF induces human neutrophil IgA-mediated phagocytosis by an IgA Fc receptor activation mechanism. Weisbart, R.H., Kacena, A., Schuh, A., Golde, D.W. Nature (1988) [Pubmed]
  22. Induction of endothelial cell expression of granulocyte and macrophage colony-stimulating factors by modified low-density lipoproteins. Rajavashisth, T.B., Andalibi, A., Territo, M.C., Berliner, J.A., Navab, M., Fogelman, A.M., Lusis, A.J. Nature (1990) [Pubmed]
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  26. Expression of colony-stimulating factor genes by normal human mesothelial cells and human malignant mesothelioma cells lines in vitro. Demetri, G.D., Zenzie, B.W., Rheinwald, J.G., Griffin, J.D. Blood (1989) [Pubmed]
  27. Rapid activation of the STAT3 transcription factor by granulocyte colony-stimulating factor. Tian, S.S., Lamb, P., Seidel, H.M., Stein, R.B., Rosen, J. Blood (1994) [Pubmed]
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  39. Recombinant human TNF alpha stimulates production of granulocyte colony-stimulating factor. Koeffler, H.P., Gasson, J., Ranyard, J., Souza, L., Shepard, M., Munker, R. Blood (1987) [Pubmed]
  40. Actions of human interleukin-4/B-cell stimulatory factor-1 on proliferation and differentiation of enriched hematopoietic progenitor cells in culture. Sonoda, Y., Okuda, T., Yokota, S., Maekawa, T., Shizumi, Y., Nishigaki, H., Misawa, S., Fujii, H., Abe, T. Blood (1990) [Pubmed]
  41. Tumor necrosis factor downregulates granulocyte-colony-stimulating factor receptor expression on human acute myeloid leukemia cells and granulocytes. Elbaz, O., Budel, L.M., Hoogerbrugge, H., Touw, I.P., Delwel, R., Mahmoud, L.A., Löwenberg, B. J. Clin. Invest. (1991) [Pubmed]
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