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Related Collections Hematopoiesis and Stem Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 January 2002, Vol. 99, No. 1, pp. 111-120 HEMATOPOIESIS Targeted disruption of the mouse colony-stimulating factor 1 receptor gene results in osteopetrosis, mononuclear phagocyte deficiency, increased primitive progenitor cell frequencies, and reproductive defects Xu-Ming Dai, Gregory R. Ryan, Andrew J. Hapel, Melissa G. Dominguez, Robert G. Russell, Sara Kapp, Vonetta Sylvestre, and E. Richard Stanley From the Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY. The effects of colony-stimulating factor 1 (CSF-1), the primary regulator of mononuclear phagocyte production, are thought to be mediated by the CSF-1 receptor (CSF-1R), encoded by the c-fms proto-oncogene. To investigate the in vivo specificity of CSF-1 for the CSF-1R, the mouse Csf1r gene was inactivated. The phenotype of Csf1/Csf1r mice closely resembled the phenotype of CSF-1-nullizygous (Csf1op/Csf1op) mice, including the osteopetrotic, hematopoietic, tissue macrophage, and reproductive phenotypes. Compared with their wild-type littermates, splenic erythroid burst-forming unit and high-proliferative potential colony-forming cell levels in both Csf1op/Csf1op and Csf1/Csf1r mice were significantly elevated, consistent with a negative regulatory role of CSF-1 in erythropoiesis and the maintenance of primitive hematopoietic progenitor cells. The circulating CSF-1 concentration in Csf1r/Csf1r mice was elevated 20-fold, in agreement with the previously reported clearance of circulating CSF-1 by CSF-1R-mediated endocytosis and intracellular destruction. Despite their overall similarity, several phenotypic characteristics of the Csf1r/Csf1r mice were more severe than those of the Csf1op/Csf1op mice. The results indicate that all of the effects of CSF-1 are mediated via the CSF-1R, but that subtle effects of the CSF-1R could result from its CSF-1-independent activation. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Hiasa, M. Abe, A. Nakano, A. Oda, H. Amou, S. Kido, K. Takeuchi, K. Kagawa, K. Yata, T. Hashimoto, et al. GM-CSF and IL-4 induce dendritic cell differentiation and disrupt osteoclastogenesis through M-CSF receptor shedding by up-regulation of TNF-{alpha} converting enzyme (TACE) Blood, November 12, 2009; 114(20): 4517 - 4526. [Abstract] [Full Text] [PDF] Y. Wittrant, Y. Gorin, S. Mohan, B. Wagner, and S. L. Abboud-Werner Colony-Stimulating Factor-1 (CSF-1) Directly Inhibits Receptor Activator of Nuclear Factor-{kappa}B Ligand (RANKL) Expression by Osteoblasts Endocrinology, November 1, 2009; 150(11): 4977 - 4988. 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