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Blood, 5 March 2009, Vol. 113, No. 10, pp. 2342-2351. Prepublished online as a Blood First Edition Paper on January 7, 2009; DOI 10.1182/blood-2008-07-168138. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2008-07-168138v1 113/10/2342    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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Li, Y. Articles by Yang, F.-C. Search for Related Content PubMed PubMed Citation Articles by Li, Y. Articles by Yang, F.-C. Related Collections Hematopoiesis and Stem Cells Transplantation Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  TRANSPLANTATION Mesenchymal stem/progenitor cells promote the reconstitution of exogenous hematopoietic stem cells in Fancg–/– mice in vivo Yan Li1,2, Shi Chen1,2, Jin Yuan1,2, Yanzhu Yang1,2, Jingling Li1,2, Jin Ma3, Xiaohua Wu1,2, Marcel Freund3, Karen Pollok1,2, Helmut Hanenberg13, W. Scott Goebel1,2, and Feng-Chun Yang1,2,4 1 Department of Pediatrics and 2 Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis; 3 Department of Pediatric Oncology, Hematology and Clinical Immunology, Children's Hospital, Heinrich Heine University, Duesseldorf, Germany; and 4 Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis Fanconi anemia (FA) is a heterogeneous genetic disorder characterized by bone marrow failure and complex congenital anomalies. Although mutations in FA genes result in a characteristic phenotype in the hematopoietic stem/progenitor cells (HSPCs), little is known about the consequences of a nonfunctional FA pathway in other stem/progenitor cell compartments. Given the intense functional interactions between HSPCs and the mesenchymalmicroenvironment, we investigated the FA pathway on the cellular functions of murine mesenchymal stem/progenitor cells (MSPCs) and their interactions with HSPCs in vitro and in vivo. Here, we show that loss of the murine homologue of FANCG (Fancg) results in a defect in MSPC proliferation and in their ability to support the adhesion and engraftment of murine syngeneic HSPCs in vitro or in vivo. Transplantation of wild-type (WT) but not Fancg–/– MSPCs into the tibiae of Fancg–/– recipient mice enhances the HSPC engraftment kinetics, the BM cellularity, and the number of progenitors per tibia of WT HSPCs injected into lethally irradiated Fancg–/– recipients. Collectively, these data show that FA proteins are required in the BM microenvironment to maintain normal hematopoiesis and provide genetic and quantitative evidence that adoptive transfer of WT MSPCs enhances hematopoietic stem cell engraftment. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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