Differentiation-linked changes in tyrosine phosphorylation, functional activity, and gene expression downstream from the granulocyte-macrophage colony-stimulating factor receptor

Blood. 1994 Aug 15;84(4):1064-73.

Abstract

The HL-60 model of myeloid maturation was used to test whether changes in signaling from the granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor accompany maturation-related changes in cellular responses to GM-CSF. Receptor expression, tyrosine phosphorylation, functional activity, and c-fos gene expression were measured. Functional GM-CSF receptors were present throughout differentiation as both uninduced and dimethyl sulfoxide (DMSO)-induced HL-60 cells responded to GM-CSF, albeit in different ways. Uninduced promyelocytes proliferated in response to GM-CSF, whereas DMSO-induced cells lost the capacity to proliferate but did respond with increased expression of beta 2-integrins, enhanced respiratory burst activity, and metabolism of arachidonic acid. GM-CSF-stimulated upregulation of c-fos mRNA expression was not detected in immature cells but developed after 2 to 4 days with DMSO in line with a marked increase in responsiveness to stimulation with phorbol ester, showing that increased expression of c-fos is predominantly a feature of mature phagocytes. GM-CSF stimulated the tyrosine phosphorylation of a broadly similar range of proteins in both uninduced and DMSO-treated HL-60 cells, but protein bands were more heavily phosphorylated in DMSO-induced cells. Phosphorylation was rapid in onset and very transient in immature cells. Phosphorylation of several proteins, in particular a 130-kD band, was more sustained in DMSO-induced cells. These differences in signaling were not because of numerical differences in receptors, because reduction of GM-CSF concentration to trigger equivalent numbers of high-affinity receptors delayed the onset of phosphorylation in DMSO-induced cells. We conclude that there are maturation-related changes in signaling downstream from the GM-CSF receptor.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Arachidonic Acid / metabolism
  • CD18 Antigens
  • Cell Differentiation / drug effects
  • Cell Differentiation / physiology*
  • Cell Division / drug effects
  • Cell Line
  • Dimethyl Sulfoxide / pharmacology
  • Gene Expression*
  • Genes, fos*
  • Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology
  • Humans
  • Integrins / biosynthesis
  • Kinetics
  • Leukemia, Promyelocytic, Acute
  • Phosphoproteins / biosynthesis
  • Phosphoproteins / metabolism
  • Phosphorylation
  • Phosphotyrosine
  • RNA, Messenger / analysis
  • RNA, Messenger / metabolism
  • Receptors, Granulocyte-Macrophage Colony-Stimulating Factor / biosynthesis*
  • Receptors, Granulocyte-Macrophage Colony-Stimulating Factor / genetics
  • Receptors, Granulocyte-Macrophage Colony-Stimulating Factor / metabolism
  • Superoxides / metabolism
  • Time Factors
  • Tumor Cells, Cultured
  • Tyrosine / analogs & derivatives*
  • Tyrosine / analysis
  • Tyrosine / metabolism

Substances

  • CD18 Antigens
  • Integrins
  • Phosphoproteins
  • RNA, Messenger
  • Receptors, Granulocyte-Macrophage Colony-Stimulating Factor
  • Superoxides
  • Phosphotyrosine
  • Arachidonic Acid
  • Tyrosine
  • Granulocyte-Macrophage Colony-Stimulating Factor
  • Dimethyl Sulfoxide