Myeloid cell proliferation stimulated by steel factor is pertussis toxin sensitive and enhanced by cholera toxin

Paul C. Hendrie, Hal Broxmeyer

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Effects of G-protein toxins on Steel factor (SLF) and granulocyte-macrophage colony stimulating factor (GM-CSF) stimulated proliferation of human factor-dependent cell line, M07e, were evaluated. Pertussis toxin pretreatment suppressed GM-CSF- or Steel factor-induced proliferation by 54±8%; however, proliferation induced by the combination of GM-CSF plus Steel factor was suppressed to a much lesser extent (14±8%). Pretreatment of M07e cells with cholera toxin, suppressed GM-CSF- and GM-CSF plus Steel factor-stimulated proliferation by 57 ± 6% and 79%, respectively, but increased the proliferative response to Steel factor alone by twofold. Similar effects of pertussis toxin and cholera toxin were observed on proliferation of normal myeloid progenitor cells from human umbilical cord blood. Pertussis toxin treatment of M07e cells for 4 h resulted in the ADP-ribosylation of 40-42 kDa protein band but did not significantly increase cyclic AMP levels. Cholera toxin pretreatment was associated with a 10-fold increase in intracellular cyclic AMP levels. These results implicate pertussis toxin sensitive pathways for both GM-CSF and Steel factor, but suggest that these pathways may not be required for synergistic proliferation stimulated by the combination. In addition, proliferation stimulated by GM-CSF, ± Steel factor, is sensitive to cholera toxin pretreatment; whereas cholera toxin pretreatment enhanced proliferation stimulated by Steel factor, possibly via increased cyclic AMP. This suggests divergent signal transduction pathways for the two cytokines.

Original languageEnglish
Pages (from-to)547-560
Number of pages14
JournalInternational Journal of Immunopharmacology
Volume16
Issue number7
DOIs
StatePublished - 1994

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Stem Cell Factor
Cholera Toxin
Pertussis Toxin
Myeloid Cells
Granulocyte-Macrophage Colony-Stimulating Factor
Cell Proliferation
Cyclic AMP
Myeloid Progenitor Cells
Fetal Blood
GTP-Binding Proteins
Adenosine Diphosphate
Signal Transduction
Cytokines
Cell Line

ASJC Scopus subject areas

  • Immunology
  • Pharmacology

Cite this

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title = "Myeloid cell proliferation stimulated by steel factor is pertussis toxin sensitive and enhanced by cholera toxin",
abstract = "Effects of G-protein toxins on Steel factor (SLF) and granulocyte-macrophage colony stimulating factor (GM-CSF) stimulated proliferation of human factor-dependent cell line, M07e, were evaluated. Pertussis toxin pretreatment suppressed GM-CSF- or Steel factor-induced proliferation by 54±8{\%}; however, proliferation induced by the combination of GM-CSF plus Steel factor was suppressed to a much lesser extent (14±8{\%}). Pretreatment of M07e cells with cholera toxin, suppressed GM-CSF- and GM-CSF plus Steel factor-stimulated proliferation by 57 ± 6{\%} and 79{\%}, respectively, but increased the proliferative response to Steel factor alone by twofold. Similar effects of pertussis toxin and cholera toxin were observed on proliferation of normal myeloid progenitor cells from human umbilical cord blood. Pertussis toxin treatment of M07e cells for 4 h resulted in the ADP-ribosylation of 40-42 kDa protein band but did not significantly increase cyclic AMP levels. Cholera toxin pretreatment was associated with a 10-fold increase in intracellular cyclic AMP levels. These results implicate pertussis toxin sensitive pathways for both GM-CSF and Steel factor, but suggest that these pathways may not be required for synergistic proliferation stimulated by the combination. In addition, proliferation stimulated by GM-CSF, ± Steel factor, is sensitive to cholera toxin pretreatment; whereas cholera toxin pretreatment enhanced proliferation stimulated by Steel factor, possibly via increased cyclic AMP. This suggests divergent signal transduction pathways for the two cytokines.",
author = "Hendrie, {Paul C.} and Hal Broxmeyer",
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T1 - Myeloid cell proliferation stimulated by steel factor is pertussis toxin sensitive and enhanced by cholera toxin

AU - Hendrie, Paul C.

AU - Broxmeyer, Hal

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N2 - Effects of G-protein toxins on Steel factor (SLF) and granulocyte-macrophage colony stimulating factor (GM-CSF) stimulated proliferation of human factor-dependent cell line, M07e, were evaluated. Pertussis toxin pretreatment suppressed GM-CSF- or Steel factor-induced proliferation by 54±8%; however, proliferation induced by the combination of GM-CSF plus Steel factor was suppressed to a much lesser extent (14±8%). Pretreatment of M07e cells with cholera toxin, suppressed GM-CSF- and GM-CSF plus Steel factor-stimulated proliferation by 57 ± 6% and 79%, respectively, but increased the proliferative response to Steel factor alone by twofold. Similar effects of pertussis toxin and cholera toxin were observed on proliferation of normal myeloid progenitor cells from human umbilical cord blood. Pertussis toxin treatment of M07e cells for 4 h resulted in the ADP-ribosylation of 40-42 kDa protein band but did not significantly increase cyclic AMP levels. Cholera toxin pretreatment was associated with a 10-fold increase in intracellular cyclic AMP levels. These results implicate pertussis toxin sensitive pathways for both GM-CSF and Steel factor, but suggest that these pathways may not be required for synergistic proliferation stimulated by the combination. In addition, proliferation stimulated by GM-CSF, ± Steel factor, is sensitive to cholera toxin pretreatment; whereas cholera toxin pretreatment enhanced proliferation stimulated by Steel factor, possibly via increased cyclic AMP. This suggests divergent signal transduction pathways for the two cytokines.

AB - Effects of G-protein toxins on Steel factor (SLF) and granulocyte-macrophage colony stimulating factor (GM-CSF) stimulated proliferation of human factor-dependent cell line, M07e, were evaluated. Pertussis toxin pretreatment suppressed GM-CSF- or Steel factor-induced proliferation by 54±8%; however, proliferation induced by the combination of GM-CSF plus Steel factor was suppressed to a much lesser extent (14±8%). Pretreatment of M07e cells with cholera toxin, suppressed GM-CSF- and GM-CSF plus Steel factor-stimulated proliferation by 57 ± 6% and 79%, respectively, but increased the proliferative response to Steel factor alone by twofold. Similar effects of pertussis toxin and cholera toxin were observed on proliferation of normal myeloid progenitor cells from human umbilical cord blood. Pertussis toxin treatment of M07e cells for 4 h resulted in the ADP-ribosylation of 40-42 kDa protein band but did not significantly increase cyclic AMP levels. Cholera toxin pretreatment was associated with a 10-fold increase in intracellular cyclic AMP levels. These results implicate pertussis toxin sensitive pathways for both GM-CSF and Steel factor, but suggest that these pathways may not be required for synergistic proliferation stimulated by the combination. In addition, proliferation stimulated by GM-CSF, ± Steel factor, is sensitive to cholera toxin pretreatment; whereas cholera toxin pretreatment enhanced proliferation stimulated by Steel factor, possibly via increased cyclic AMP. This suggests divergent signal transduction pathways for the two cytokines.

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