C/EBPalpha deficiency results in hyperproliferation of hematopoietic progenitor cells and disrupts macrophage development in vitro and in vivo

Blood. 2004 Sep 15;104(6):1639-47. doi: 10.1182/blood-2003-11-3963. Epub 2004 Apr 8.

Abstract

CCAAT enhancer binding protein-alpha (C/EBPalpha) inhibits proliferation in multiple cell types; therefore, we evaluated whether C/EBPalpha-deficient hematopoietic progenitor cells (HPCs) have an increased proliferative potential in vitro and in vivo. In this study we demonstrate that C/EBPalpha(-/-) fetal liver (FL) progenitors are hyperproliferative, show decreased differentiation potential, and show increased self-renewal capacity in response to hematopoietic growth factors (HGFs). There are fewer committed bipotential progenitors in C/EBPalpha(-/-) FL, whereas multipotential progenitors are unaffected. HGF-dependent progenitor cell lines can be derived by directly culturing C/EBPalpha(-/-) FL cells in vitro Hyperproliferative spleen colonies and myelodysplastic syndrome (MDS) are observed in mice reconstituted with C/EBPalpha(-/-) FL cells, indicating progenitor hyperproliferation in vitro and in vivo. C/EBPalpha(-/-) FL lacked macrophage progenitors in vitro and had impaired ability to generate macrophages in vivo. These findings show that C/EBPalpha deficiency results in hyperproliferation of HPCs and a block in the ability of multipotential progenitors to differentiate into bipotential granulocyte/macrophage progenitors and their progeny.

Publication types

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

MeSH terms

  • Animals
  • CCAAT-Enhancer-Binding Protein-alpha / deficiency*
  • CCAAT-Enhancer-Binding Protein-alpha / genetics
  • CCAAT-Enhancer-Binding Protein-alpha / metabolism
  • Cell Differentiation* / drug effects
  • Cell Division / drug effects
  • Cell Transplantation
  • Cells, Cultured
  • Gene Deletion
  • Gene Expression Regulation, Developmental
  • Hematopoietic Stem Cells / drug effects
  • Hematopoietic Stem Cells / metabolism*
  • Hematopoietic Stem Cells / pathology*
  • Hepatocyte Growth Factor / pharmacology
  • Interleukin-3 / metabolism
  • Liver / embryology
  • Liver / metabolism
  • Liver / pathology
  • Macrophages / drug effects
  • Macrophages / metabolism*
  • Macrophages / pathology*
  • Mice
  • Mice, Knockout
  • Proto-Oncogene Proteins c-met / genetics
  • Proto-Oncogene Proteins c-met / metabolism
  • Survival Rate

Substances

  • CCAAT-Enhancer-Binding Protein-alpha
  • Interleukin-3
  • Hepatocyte Growth Factor
  • Proto-Oncogene Proteins c-met