The glucocorticoid receptor is required for stress erythropoiesis

  1. Anton Bauer,
  2. Francois Tronche,
  3. Oliver Wessely,
  4. Christoph Kellendonk,
  5. Holger M. Reichardt,
  6. Peter Steinlein,
  7. Günther Schütz, and
  8. Hartmut Beug
  1. Research Institute of Molecular Pathology (IMP), Dr. Bohr-Gasse 7, A-1030 Vienna, Austria; Molecular Biology of the Cell I, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany

Abstract

The glucocorticoid receptor (GR) coordinates a multitude of physiological responses in vivo. In vitro, glucocorticoids are required for sustained proliferation of erythroid progenitors (ebls). Here, we analyze the impact of the GR on erythropoiesis in vivo, using GR-deficient mice or mice expressing a GR defective for transactivation. In vitro, sustained proliferation of primary ebls requires an intact GR. In vivo, the GR is required for rapid expansion of ebls under stress situations like erythrolysis or hypoxia. A particular, GR-sensitive progenitor could be identified as being responsible for the stress response. Thus, GR-mediated regulation of ebl proliferation is essential for stress erythropoiesis in vivo.

Keywords

Footnotes

  • Present address: Howard Hughes Medical Institute, University of California, Los Angeles (UCLA), Los Angeles, California 90095-1662 USA.

  • Corresponding author.

  • E-MAIL g.schuetz{at}dkfz-heidelberg.de; FAX +49-6221-423470.

    • Received July 28, 1999.
    • Accepted September 21, 1999.
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