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Blood, 1 May 2004, Vol. 103, No. 9, pp. 3258-3264. Prepublished online as a Blood First Edition Paper on January 15, 2004; DOI 10.1182/blood-2003-11-4011. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-11-4011v1 103/9/3258    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 Visnjic, D. Articles by Aguila, H. L. Search for Related Content PubMed PubMed Citation Articles by Visnjic, D. Articles by Aguila, H. L. Related Collections Hematopoiesis and Stem Cells Plenary Papers Free Research Articles Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  PLENARY PAPERS Hematopoiesis is severely altered in mice with an induced osteoblast deficiency Dora Visnjic, Zana Kalajzic, David W. Rowe, Vedran Katavic, Joseph Lorenzo, and Hector L. Aguila From the Department of Genetics and Developmental Biology; Division of Endocrinology, Department of Medicine; and Center for Immunotherapy of Cancer and Infectious Diseases, Department of Medicine, University of Connecticut Health Center, Farmington. We previously reported a transgenic mouse model expressing herpesvirus thymidine kinase (TK) gene under the control of a 2.3-kilobase fragment of the rat collagen 1 type I promoter (Col2.3TK). This construct confers lineage-specific expression in developing osteoblasts, allowing the conditional ablation of osteoblast lineage after treatment with ganciclovir (GCV). After GCV treatment these mice have profound alterations on bone formation leading to a progressive bone loss. In addition, treated animals also lose bone marrow cellularity. In this report we characterized hematopoietic parameters in GCV-treated Col2.3TK mice, and we show that after treatment transgenic animals lose lymphoid, erythroid, and myeloid progenitors in the bone marrow, followed by decreases in the number of hematopoietic stem cells (HSCs). Together with the decrease in bone marrow hematopoiesis, active extramedullary hematopoiesis was observed in the spleen and liver, as measured by an increase in peripheral HSCs and active primary in vitro hematopoiesis. After withdrawal of GCV, osteoblasts reappeared in the bone compartment together with a recovery of medullary and decrease in extramedullary hematopoiesis. These observations directly demonstrate the role of osteoblasts in hematopoiesis and provide a model to study the interactions between the mesenchymal and hematopoietic compartments in the marrow. (Blood. 2004; 103:3258-3264) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Osteoblasts make for good neighbors Robert F. Klein Blood 2004 103: 3247. [Full Text] [PDF] This article has been cited by other articles: M. J. Nemeth, K. K. Mak, Y. Yang, and D. M. Bodine {beta}-Catenin Expression in the Bone Marrow Microenvironment Is Required for Long-Term Maintenance of Primitive Hematopoietic Cells Stem Cells, May 1, 2009; 27(5): 1109 - 1119. [Abstract] [Full Text] [PDF] J. Lorenzo, M. Horowitz, and Y. 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