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C/EBP alpha determines hematopoietic cell fate in multipotential progenitor cells by inhibiting erythroid differentiation and inducing myeloid differentiation

  1. Author:
    Suh, H. C.
    Gooya, J.
    Renn, K.
    Friedman, A. D.
    Johnson, P. F.
    Keller, J. R.

  2. Author Address

    SAIC Frederick, Natl Canc Inst, Basic Res Program, Canc Res Ctr, Frederick, MD 20702 USA. Johns Hopkins Univ, Div Pediat Oncol, Baltimore, MD USA. NCI, Lab Prot Dynam & Signaling, Canc Res Ctr, Frederick, MD 21701 USA.;Keller, JR, SAIC Frederick, Natl Canc Inst, Basic Res Program, Canc Res Ctr, Bldg 560,Rm 12-03, Frederick, MD 20702 USA.;kellerj@ncifcrf.gov
    1. Year: 2006
    2. Date: Jun
  2. Journal: Blood
    1. 107
    2. 11
    3. Pages: 4308-4316
  4. Type of Article: Article
  5. ISSN: 0006-4971
  1. Abstract:

    C/EBP alpha is an essential transcription factor required for myeloid differentiation. While C/EBP alpha can act as a cell fate switch to promote granulocyte differentiation in bipotential granulocyte-macrophage progenitors (GMPs), its role in regulating cell fate decisions in more primitive progenitors is not known. We found increased numbers of erythroid progenitors and erythroid cells in C/EBP alpha(-/-) fetal liver (FL). Also, enforced expression of C/EBP alpha in hematopoietic stem cells resulted in a loss of erythroid progenitors and an increase in myeloid cells by inhibition of erythroid development and inducing myeloid differentiation. Conditional expression of C/EBPa in murine erythroleukemia (MEL) cells induced myeloid-specific genes, while inhibiting erythroid-specific gene expression including erythropoietin receptor (EpoR), which suggests a novel mechanism to determine hematopoietic cell fate. Thus, C/EBP alpha functions in hematopoietic cell fate decisions by the dual actions of inhibiting erythroid and inducing myeloid gene expression in multipotential progenitors.

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External Sources

  1. View record in Web of Science®
  2. WOS: 000237877300024

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