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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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HEMATOPOIESIS AND STEM CELLS

Impaired response to GM-CSF and G-CSF, and enhanced apoptosis in C/EBPβ-deficient hematopoietic cells

Tadayuki Akagi1, Takayuki Saitoh1, James O'Kelly1, Shizuo Akira2, Adrian F. Gombart1, and H. Phillip Koeffler1

1 Division of Hematology and Oncology, Cedars-Sinai Medical Center, University of California Los Angeles School of Medicine; and 2 Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan

Transcription factors known as CCAAT enhancer binding proteins (C/EBPs) are involved in hematopoietic differentiation, including myelopoiesis and granulopoiesis. C/EBPβ-deficient mice develop normally; however, they exhibit defective macrophage function, resulting in increased susceptibility to infection. Little is known about the role of C/EBPβ in granulopoiesis; therefore, we examined granulopoiesis in C/EBPβ-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/EBPβ-deficient mice. Interestingly, the hematopoietic progenitor cells of C/EBPβ-deficient mice did not respond normally to granulocyte/macrophage-colony stimulating factor and granulocyte colony stimulating factor. In addition, C/EBPβ-deficient neutrophils displayed enhanced apoptosis compared with wild-type neutrophils. Our present results indicate that C/EBPβ helps regulate survival of neutrophils, downstream of the granulocyte colony stimulating factor 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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