Synergistic induction of phospholipid metabolism by granulocyte-macrophage colony stimulating factor and steel factor in human growth factor-dependent cell line, M07e

C. Mantel, Z. Luo, Hal Broxmeyer

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6 Citations (Scopus)

Abstract

Steel factor (SLF), the ligand for the c-kit protooncogene tyrosine kinase receptor, synergizes with several hematopoietic growth factors to produce greatly enhanced proliferation of normal human hematopoietic progenitor cells as well as that of the human growth factor-dependent myeloid cell line, M07e. The mechanisms of this phenomenon remain unknown. In an attempt to understand the cellular processes relevant to this phenomenon, we examined the effects of SLF and granulocyte-macrophage colony-stimulating factor (GM-CSF) on induced lipid metabolism in M07e cells. We find that both GM-CSF and SLF induced increased phosphatidylcholine (PC) turnover rates (biosynthesis and degradation) as measured by increased [3H]-choline labelling, with SLF being more potent stimulation. The labelling of aqueous intermediates of PC metabolism was also increased by cytokine stimulation, most notably phosphocholine. Simultaneous stimulation with GM-CSF plus SLF resulted in a true synergistic induction of PC, lysoPC, and phosphocholine labelling. GM-CSF and SLF each induced asymmetric labelling of various phospholipid classes as measured by incorporation of different [3H]-fatty acids. [3H]-myristic acid labelling of phosphatidylserine was most prominently induced (approximately 12-fold). Cytosolic choline kinase activity was also upregulated more than twofold over control by SLF, which might contribute to the increased phosphocholine labelling. These effects may have relevance to the intracellular mechanisms of the synergistic proliferative stimulation of SLF plus GM-CSF on M07e cells.

Original languageEnglish
Pages (from-to)641-647
Number of pages7
JournalLipids
Volume30
Issue number7
DOIs
StatePublished - Jul 1995

Fingerprint

granulocyte-macrophage colony-stimulating factor
Stem Cell Factor
human growth
Granulocyte-Macrophage Colony-Stimulating Factor
steel
Metabolism
growth factors
Phospholipids
Intercellular Signaling Peptides and Proteins
phospholipids
Cells
cell lines
Cell Line
Labeling
metabolism
Phosphorylcholine
phosphatidylcholines
Phosphatidylcholines
choline kinase
Choline Kinase

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Biochemistry
  • Biochemistry, Genetics and Molecular Biology(all)
  • Food Science

Cite this

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title = "Synergistic induction of phospholipid metabolism by granulocyte-macrophage colony stimulating factor and steel factor in human growth factor-dependent cell line, M07e",
abstract = "Steel factor (SLF), the ligand for the c-kit protooncogene tyrosine kinase receptor, synergizes with several hematopoietic growth factors to produce greatly enhanced proliferation of normal human hematopoietic progenitor cells as well as that of the human growth factor-dependent myeloid cell line, M07e. The mechanisms of this phenomenon remain unknown. In an attempt to understand the cellular processes relevant to this phenomenon, we examined the effects of SLF and granulocyte-macrophage colony-stimulating factor (GM-CSF) on induced lipid metabolism in M07e cells. We find that both GM-CSF and SLF induced increased phosphatidylcholine (PC) turnover rates (biosynthesis and degradation) as measured by increased [3H]-choline labelling, with SLF being more potent stimulation. The labelling of aqueous intermediates of PC metabolism was also increased by cytokine stimulation, most notably phosphocholine. Simultaneous stimulation with GM-CSF plus SLF resulted in a true synergistic induction of PC, lysoPC, and phosphocholine labelling. GM-CSF and SLF each induced asymmetric labelling of various phospholipid classes as measured by incorporation of different [3H]-fatty acids. [3H]-myristic acid labelling of phosphatidylserine was most prominently induced (approximately 12-fold). Cytosolic choline kinase activity was also upregulated more than twofold over control by SLF, which might contribute to the increased phosphocholine labelling. These effects may have relevance to the intracellular mechanisms of the synergistic proliferative stimulation of SLF plus GM-CSF on M07e cells.",
author = "C. Mantel and Z. Luo and Hal Broxmeyer",
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T1 - Synergistic induction of phospholipid metabolism by granulocyte-macrophage colony stimulating factor and steel factor in human growth factor-dependent cell line, M07e

AU - Mantel, C.

AU - Luo, Z.

AU - Broxmeyer, Hal

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N2 - Steel factor (SLF), the ligand for the c-kit protooncogene tyrosine kinase receptor, synergizes with several hematopoietic growth factors to produce greatly enhanced proliferation of normal human hematopoietic progenitor cells as well as that of the human growth factor-dependent myeloid cell line, M07e. The mechanisms of this phenomenon remain unknown. In an attempt to understand the cellular processes relevant to this phenomenon, we examined the effects of SLF and granulocyte-macrophage colony-stimulating factor (GM-CSF) on induced lipid metabolism in M07e cells. We find that both GM-CSF and SLF induced increased phosphatidylcholine (PC) turnover rates (biosynthesis and degradation) as measured by increased [3H]-choline labelling, with SLF being more potent stimulation. The labelling of aqueous intermediates of PC metabolism was also increased by cytokine stimulation, most notably phosphocholine. Simultaneous stimulation with GM-CSF plus SLF resulted in a true synergistic induction of PC, lysoPC, and phosphocholine labelling. GM-CSF and SLF each induced asymmetric labelling of various phospholipid classes as measured by incorporation of different [3H]-fatty acids. [3H]-myristic acid labelling of phosphatidylserine was most prominently induced (approximately 12-fold). Cytosolic choline kinase activity was also upregulated more than twofold over control by SLF, which might contribute to the increased phosphocholine labelling. These effects may have relevance to the intracellular mechanisms of the synergistic proliferative stimulation of SLF plus GM-CSF on M07e cells.

AB - Steel factor (SLF), the ligand for the c-kit protooncogene tyrosine kinase receptor, synergizes with several hematopoietic growth factors to produce greatly enhanced proliferation of normal human hematopoietic progenitor cells as well as that of the human growth factor-dependent myeloid cell line, M07e. The mechanisms of this phenomenon remain unknown. In an attempt to understand the cellular processes relevant to this phenomenon, we examined the effects of SLF and granulocyte-macrophage colony-stimulating factor (GM-CSF) on induced lipid metabolism in M07e cells. We find that both GM-CSF and SLF induced increased phosphatidylcholine (PC) turnover rates (biosynthesis and degradation) as measured by increased [3H]-choline labelling, with SLF being more potent stimulation. The labelling of aqueous intermediates of PC metabolism was also increased by cytokine stimulation, most notably phosphocholine. Simultaneous stimulation with GM-CSF plus SLF resulted in a true synergistic induction of PC, lysoPC, and phosphocholine labelling. GM-CSF and SLF each induced asymmetric labelling of various phospholipid classes as measured by incorporation of different [3H]-fatty acids. [3H]-myristic acid labelling of phosphatidylserine was most prominently induced (approximately 12-fold). Cytosolic choline kinase activity was also upregulated more than twofold over control by SLF, which might contribute to the increased phosphocholine labelling. These effects may have relevance to the intracellular mechanisms of the synergistic proliferative stimulation of SLF plus GM-CSF on M07e cells.

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