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 Blood, 15 March 2008, Vol. 111, No. 6, pp. 2999-3004.
Prepublished online as a Blood First Edition Paper on December 4, 2007; DOI 10.1182/blood-2007-04-087213.

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Submitted April 25, 2007
Accepted November 20, 2007

Impaired response to GM-CSF and G-CSF, and enhanced apoptosis in C/EBP{beta}-deficient hematopoietic cells

Tadayuki Akagi*, Takayuki Saitoh, James O'Kelly, Shizuo Akira, Adrian F Gombart, and H. Phillip Koeffler

Division of Hematology and Oncology, Cedars-Sinai Medical Center, UCLA School of Medicine, Los Angeles, CA, United States
Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan

* Corresponding author; email: akagit{at}cshs.org.

Transcription factors known as CCAAT enhancer binding proteins (C/EBPs) are involved in hematopoietic differentiation including myelopoiesis and granulopoiesis. C/EBP{beta}-deficient mice develop normally; however, they exhibit defective macrophage function, resulting in increased susceptibility to infection. Little is known about the role of C/EBP{beta} in granulopoiesis; therefore, we examined granulopoiesis in C/EBP{beta}-deficient mice. Morphology, the number of peripheral blood- and bone marrow-cells, and the expression of genes specific for the myeloid lineage were normal in C/EBP{beta}-deficient mice. Interestingly, the hematopoietic progenitor cells of C/EBP{beta}-deficient mice did not respond normally to GM-CSF and G-CSF. In addition, C/EBP{beta}-deficient neutrophils displayed enhanced apoptosis compared with wild-type neutrophils. Our present results indicate that C/EBP{beta} helps regulate survival of neutrophils, downstream of the G-CSF receptor.


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Related Article in Blood Online:

The hidden faces of C/EBPβ
Carsten Müller-Tidow and Steffen Koschmieder
Blood 2008 111: 2949-2950. [Full Text] [PDF]



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