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Blood, 1 February 2004, Vol. 103, No. 3, pp. 1114-1123. Prepublished online as a Blood First Edition Paper on October 2, 2003; DOI 10.1182/blood-2003-08-2739. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-08-2739v1 103/3/1114    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Dai, X.-M. Articles by Stanley, E. R. Search for Related Content PubMed PubMed Citation Articles by Dai, X.-M. Articles by Stanley, E. R. Related Collections Hematopoiesis and Stem Cells Phagocytes Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  PHAGOCYTES Incomplete restoration of colony-stimulating factor 1 (CSF-1) function in CSF-1–deficient Csf1op/Csf1op mice by transgenic expression of cell surface CSF-1 Xu-Ming Dai, Xiao-Hua Zong, Vonetta Sylvestre, and E. Richard Stanley From the Departments of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY. The primary macrophage growth factor, colony-stimulating factor 1 (CSF-1), is expressed as a secreted glycoprotein or proteoglycan found in the circulation or as a biologically active cell surface glycoprotein (csCSF-1). To investigate the in vivo roles of csCSF-1, we created mice that exclusively express csCSF-1, in a normal tissue-specific and developmental manner, by transgenic expression of csCSF-1 in the CSF-1-deficient osteopetrotic (Csf1op/Csf1op) background. The gross defects of Csf1op/Csf1op mice, including growth retardation, failure of tooth eruption, and abnormal male and female reproductive functions were corrected. Macrophage densities in perinatal liver, bladder, sublinguinal salivary gland, kidney cortex, dermis, and synovial membrane were completely restored, whereas only partial or no restoration was achieved in adult liver, adrenal gland, kidney medulla, spleen, peritoneal cavity, and intestine. Residual osteopetrosis, significantly delayed trabecular bone resorption in the subepiphyseal region of the long bone, and incomplete correction of the hematologic abnormalities in the peripheral blood, bone marrow, and spleens of CSF-1-deficient mice were also found in mice exclusively expressing csCSF-1. These data suggest that although csCSF-1 alone is able to normalize several aspects of development in Csf1op/Csf1op mice, it cannot fully restore in vivo CSF-1 function, which requires the presence of the secreted glycoprotein and/or proteoglycan forms. (Blood. 2004;103:1114-1123) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K. Horiuchi, H. Morioka, H. Takaishi, H. Akiyama, C. P. Blobel, and Y. Toyama Ectodomain Shedding of FLT3 Ligand Is Mediated by TNF-{alpha} Converting Enzyme J. Immunol., June 15, 2009; 182(12): 7408 - 7414. [Abstract] [Full Text] [PDF] L. Wang, G.-G. Zheng, C.-H. Ma, Y.-M. Lin, H.-Y. Zhang, Y.-Y. Ma, J.-H. Chong, and K.-F. Wu A Special Linker between Macrophage and Hematopoietic Malignant Cells: Membrane Form of Macrophage Colony-Stimulating Factor Cancer Res., July 15, 2008; 68(14): 5639 - 5647. [Abstract] [Full Text] [PDF] S. Aharinejad, D. Abraham, P. Paulus, K. Zins, M. 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