| First Author | Akagi T | Year | 2008 |
| Journal | Blood | Volume | 111 |
| Issue | 6 | Pages | 2999-3004 |
| PubMed ID | 18056834 | Mgi Jnum | J:132721 |
| Mgi Id | MGI:3776722 | Doi | 10.1182/blood-2007-04-087213 |
| Citation | Akagi T, et al. (2008) Impaired response to GM-CSF and G-CSF, and enhanced apoptosis in C/EBP{beta}-deficient hematopoietic cells. Blood 111(6):2999-3004 |
| abstractText | Transcription factors known as CCAAT enhancer binding proteins (C/EBPs) are involved in hematopoietic differentiation, including myelopoiesis and granulopoiesis. C/EBPbeta-deficient mice develop normally; however, they exhibit defective macrophage function, resulting in increased susceptibility to infection. Little is known about the role of C/EBPbeta in granulopoiesis; therefore, we examined granulopoiesis in C/EBPbeta-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/EBPbeta-deficient mice. Interestingly, the hematopoietic progenitor cells of C/EBPbeta-deficient mice did not respond normally to granulocyte/macrophage-colony stimulating factor and granulocyte colony stimulating factor. In addition, C/EBPbeta-deficient neutrophils displayed enhanced apoptosis compared with wild-type neutrophils. Our present results indicate that C/EBPbeta helps regulate survival of neutrophils, downstream of the granulocyte colony stimulating factor receptor. |
