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Blood, 15 December 2005, Vol. 106, No. 13, pp. 4093-4101. Prepublished online as a Blood First Edition Paper on August 23, 2005; DOI 10.1182/blood-2005-02-0671. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 2005-02-0671v1 106/13/4093    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 Yao, L. Articles by McEver, R. P. Search for Related Content PubMed PubMed Citation Articles by Yao, L. Articles by McEver, R. P. Related Collections Hematopoiesis and Stem Cells Hemostasis, Thrombosis, and Vascular Biology Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Bone marrow dysfunction in mice lacking the cytokine receptor gp130 in endothelial cells Longbiao Yao, Takafumi Yokota, Lijun Xia, Paul W. Kincade, and Rodger P. McEver From the Cardiovascular Biology Research Program and the Immunobiology and Cancer Program, Oklahoma Medical Research Foundation, Oklahoma City, OK; and the Departments of Microbiology and Immunology and of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK. In vitro studies suggest that bone marrow endothelial cells contribute to multilineage hematopoiesis, but this function has not been studied in vivo. We used a Cre/loxP-mediated recombination to produce mice that lacked the cytokine receptor subunit gp130 in hematopoietic and endothelial cells. Although normal at birth, the mice developed bone marrow dysfunction that was accompanied by splenomegaly caused by extramedullary hematopoiesis. The hypocellular marrow contained myeloerythroid progenitors and functional repopulating stem cells. However, long-term bone marrow cultures produced few hematopoietic cells despite continued expression of gp130 in most stromal cells. Transplanting gp130-deficient bone marrow into irradiated wild-type mice conferred normal hematopoiesis, whereas transplanting wild-type bone marrow into irradiated gp130-deficient mice did not cure the hematopoietic defects. These data provide evidence that gp130 expression in the bone marrow microenvironment, most likely in endothelial cells, makes an important contribution to hematopoiesis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. Seita, M. Asakawa, J. Ooehara, S.-i. Takayanagi, Y. Morita, N. Watanabe, K. Fujita, M. Kudo, J. Mizuguchi, H. Ema, et al. Interleukin-27 directly induces differentiation in hematopoietic stem cells Blood, February 15, 2008; 111(4): 1903 - 1912. [Abstract] [Full Text] [PDF] W. B. Slayton, X.-M. Li, J. Butler, S. M. Guthrie, M. L. Jorgensen, J. R. Wingard, and E. W. Scott The Role of the Donor in the Repair of the Marrow Vascular Niche Following Hematopoietic Stem Cell Transplant Stem Cells, November 1, 2007; 25(11): 2945 - 2955. [Abstract] [Full Text] [PDF]

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