Upregulation of interleukin 6 and granulocyte colony-stimulating factor receptors by transcription factor CCAAT enhancer binding protein alpha (C/EBP alpha) is critical for granulopoiesis

J Exp Med. 1998 Sep 21;188(6):1173-84. doi: 10.1084/jem.188.6.1173.

Abstract

Cytokines stimulate granulopoiesis through signaling via receptors whose expression is controlled by lineage-specific transcription factors. Previously, we demonstrated that granulocyte colony-stimulating factor (G-CSF) receptor mRNA was undetectable and granulocyte maturation blocked in CCAAT enhancer binding protein alpha (C/EBPalpha)-deficient mice. This phenotype is distinct from that of G-CSF receptor-/- mice, suggesting that other genes are likely to be adversely affected by loss of C/EBPalpha. Here we demonstrate loss of interleukin 6 (IL-6) receptor and IL-6-responsive colony-forming units (CFU-IL6) in C/EBPalpha-/- mice. The observed failure of granulopoiesis could be rescued by the addition of soluble IL-6 receptor and IL-6 or by retroviral transduction of G-CSF receptors, demonstrating that loss of both of these receptors contributes to the absolute block in granulocyte maturation observed in C/EBPalpha-deficient hematopoietic cells. The results of these and other studies suggest that additional C/EBPalpha target genes, possibly other cytokine receptors, are also important for the block in granulocyte differentiation observed in vivo in C/EBPalpha-deficient mice.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • CCAAT-Enhancer-Binding Proteins
  • Cell Differentiation / genetics
  • Colony-Forming Units Assay
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • DNA-Binding Proteins / physiology*
  • Drug Synergism
  • Enhancer Elements, Genetic
  • Fetus
  • Granulocytes / physiology*
  • Hematopoiesis* / drug effects
  • Hematopoiesis* / genetics
  • Hematopoietic Stem Cells / drug effects
  • Hematopoietic Stem Cells / metabolism
  • Humans
  • Interleukin-6 / pharmacology
  • Liver / cytology
  • Liver / drug effects
  • Liver / physiology
  • Mice
  • Mice, Knockout
  • Mutation
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism
  • Nuclear Proteins / physiology*
  • RNA, Messenger / antagonists & inhibitors
  • RNA, Messenger / biosynthesis
  • Receptors, Granulocyte Colony-Stimulating Factor / antagonists & inhibitors
  • Receptors, Granulocyte Colony-Stimulating Factor / biosynthesis*
  • Receptors, Granulocyte Colony-Stimulating Factor / deficiency
  • Receptors, Granulocyte Colony-Stimulating Factor / genetics
  • Receptors, Interleukin-6 / antagonists & inhibitors
  • Receptors, Interleukin-6 / biosynthesis*
  • Receptors, Interleukin-6 / deficiency
  • Receptors, Interleukin-6 / genetics
  • Solubility
  • Transcription Factors / genetics
  • Transcription Factors / physiology*
  • Up-Regulation / genetics
  • Up-Regulation / physiology*

Substances

  • CCAAT-Enhancer-Binding Proteins
  • DNA-Binding Proteins
  • Interleukin-6
  • Nuclear Proteins
  • RNA, Messenger
  • Receptors, Granulocyte Colony-Stimulating Factor
  • Receptors, Interleukin-6
  • Transcription Factors